Category: Circulation

Ultrasound-Guided Vascular Access (2025)

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by Zackary Funk & Petra Duran-Gehring

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Introduction

Ultrasound (US) guidance has become an increasingly common technique for vascular access in the Emergency Department (ED), with applications for both central and peripheral lines [1-4]. Initially adopted for central venous catheter (CVC) insertion, particularly in the internal jugular vein, US improved placement success rates, decreased complication rates, and shortened insertion times. As US technology and training advanced, its use expanded to peripheral intravenous line (PIV) placement, where studies have demonstrated increased success rates, reduced complications, and less pain, especially for patients with difficult access [1-4]. Difficult IV access, occurring in 10% to 30% of ED patients—particularly those with morbid obesity, IV drug use, hypovolemia, or chronic illness—can delay cannulation due to multiple failed attempts [5]. Ultrasound-guided PIV placement can mitigate these challenges, with one study reporting an 85% reduction in the need for CVCs in non-critical patients through the implementation of a US-guided PIV catheter program [6]. The overall benefits of US-guided vascular access include improved success rates, fewer complications, decreased pain, reduced time to cannulation, fewer attempts required, and improved patient satisfaction [1-4]. While it may add some complexity compared to landmark or “blind” approaches, the ability to directly visualize target vessels makes US-guided vascular access a highly effective and patient-centered technique.

Indications

Intravenous (IV) access is often critically important for many aspects of patient care in the ED [1-3]. These include:

US-Guided Peripheral IV Access:

  1. Patients who have had three or more blind attempts without successful cannulation.
  2. Patients with a history of difficult IV access.
    • Always evaluate the patient using traditional visual inspection and palpation before preparing for US-guided peripheral IV access. Factors that contributed to difficult IV access during previous encounters, such as hypovolemia, may not be present during subsequent visits.
  3. Patients who have previously required central line placement solely for IV access.
    • As mentioned above, when the clinical situation permits, patients with a history of requiring US-guided vascular access should be evaluated for landmark-based IV sites and/or US-guided peripheral IV sites before proceeding to the more invasive procedure of central venous access.

US-Guided Central Venous Access:
Whenever possible, it is highly recommended to use ultrasound guidance for invasive vascular access procedures, such as central venous cannulation, due to its demonstrated ability to decrease the occurrence of severe complications and increase success rates. The primary indication for ultrasound guidance in central venous access is the need for central venous access itself. Below is a list of specific indications for central venous access [1-4]:

  1. Inability to obtain peripheral IV access required for critical interventions or investigations.
  2. Long-term administration of vasoactive substances (e.g., norepinephrine/epinephrine infusions).
  3. Administration of high-concentration or potentially caustic medications (e.g., hypertonic saline, concentrated or large volumes of potassium chloride).
  4. High-pressure or large-volume infusions, such as massive transfusions in trauma patients with hemorrhagic shock.
  5. Emergent dialysis or plasmapheresis access in patients without established arteriovenous fistulas or other dialysis-capable access.
  6. Transvenous pacemaker placement.

Contraindications

Although there are many benefits of US-guided venous access, some contraindications and considerations should be kept in mind [3,4,7]:

  1. Presence of cellulitis, burns, massive edema, or injuries at or proximal to the proposed insertion sites.
  2. Other injuries, diseases, or anatomical distortions of the affected limb/site that may lead to complications during or after access (e.g., compartment syndrome, extravasation, bleeding from neoplasms, etc.).
  3. Risk of compromised vascular flow distal to the site.
  4. Coagulopathy (considered a relative contraindication).
  5. A capacitated patient declines to undergo the procedure after demonstrating an understanding of the risks and benefits as explained by the care team.

Equipment and Patient Preparation

While the materials and equipment required for peripheral IV access are very similar to those needed for central vascular access, we have separated them into two lists to highlight some key differences. Regardless of the procedure, adherence to hand hygiene practices and the universal use of personal protective equipment are absolutely essential for every procedure.

Equipment for Peripheral IV Access

  • Ultrasound machine equipped with a high-frequency linear probe.
  • Examination gloves.
  • Skin disinfectant (e.g., alcohol swabs, chlorhexidine swabs, povidone-iodine, etc.).
  • Occlusive ultrasound probe cover.
  • Sterile ultrasound gel.
  • Elastic tourniquet.
  • IV catheter.
  • IV securement device and dressing.
  • IV extension tubing and IV port.
  • Normal saline flush.
  • Sharps disposal device/container.
  • Stool or chair (recommended).
Figure 1 - Equipment for Peripheral IV Access

Equipment for Central Venous Access

  1. Ultrasound machine with a high-frequency linear probe.
  2. Sterile gloves.
  3. Eye protection.
  4. Central Venous Catheter Kit (if available), which often includes:
    • Sterile gown.
    • Face mask.
    • Bouffant or scrub cap.
    • Skin disinfectant swabs (e.g., chlorhexidine, povidone-iodine, etc.).
    • Vial of local anesthetic, needle, and syringe.
    • 18-gauge introducer needle and syringe.
    • #11-blade scalpel.
    • Gauze.
    • Guidewire.
    • Dilator(s).
    • Central venous catheter.
    • Sterile saline flush syringes.
    • Needle driver.
    • Suture.
    • Dressing.
    • Sharps disposal hub.
  5. Sterile occlusive ultrasound probe cover sheath.
  6. Sterile ultrasound gel.
  7. IV ports.

Patient Preparation

Proper patient preparation is essential to ensure the accuracy of line placement and minimize patient discomfort or complications. 

Introduction and Identification
Begin by introducing yourself to the patient and confirming their full name. 

Patient History and Consent
Inquire about any allergies, phobias, or a history of fainting during previous IV line procedures. Clearly explain the purpose, benefits, and potential risks of the procedure in simple terms. Once the patient or their next of kin fully understands the information, obtain verbal consent. Note that written consent is not required in emergency situations unless mandated by institutional policy.

Alleviating Anxiety
Address any patient concerns and provide reassurance to help alleviate fear or anxiety. Ensuring the patient is calm can significantly improve their experience and the procedure’s success.

Procedure Steps

Here, we will describe the procedural steps for both ultrasound-guided peripheral intravenous access and ultrasound-guided central vascular access. For each procedure, ensure that the ultrasound machine and probes are in good working order and that there is sufficient power or a reliable power source to successfully and safely complete the procedure. Ultrasound probes should be disinfected before and after each use to protect both patients and providers from exposure to bloodborne and other pathogens, even when sterile probe covers are used. For an overview of the procedural steps for ultrasound-guided peripheral IV access, please review the accompanying video.

Image Acquisition in Vascular Access Procedures

Optimizing the image of the target vessel is critical for procedural safety and success in ultrasound-guided vascular access. This section will describe the general principles and equipment needed to obtain and optimize target visualization.

The high-frequency linear ultrasound probe is most commonly used for vascular access procedures as it provides high-resolution images of superficial structures in the body (Figure 2). Although this resolution comes at the cost of limited penetration into deeper tissues, this limitation is rarely an issue due to specific factors influencing the appropriate depth of target vessels for cannulation, as discussed below.

Figure 2 - Linear Probe (transducer)

The next step is to ensure proper left-right probe orientation. This is accomplished prior to image acquisition by aligning the probe indicator on the ultrasound screen with the probe indicator on the linear probe itself. According to standard convention, the probe indicator on the device screen will appear as a dot, arrow, manufacturer logo, or other marking on the upper left side of the screen (Figure 3a).

Figure 3a - US Probe and Screen Markers

The image nearest the probe indicator on the screen corresponds to the signal emitted from the probe transducer head closest to the physical probe indicator, typically a raised marking or similar feature. A simple technique to confirm orientation involves applying a small amount of ultrasound gel to one side of the probe face, touching this area with a gloved finger, and observing where the movement appears on the screen (Video 1). Once the two markers are aligned, rightward movement on the screen will correspond to movement away from the probe indicator in physical space.

Once orientation is established, perform a survey scan of the site. After applying an elastic tourniquet (if peripheral IV access is being attempted), position the probe perpendicular to the long axis of the extremity or the anticipated course of the target vessel (Figure 4).

Figure 4 - positioning the probe perpendicular to the long axis

This generates a “transverse,” “short-axis,” or “cross-sectional” image of the vessel. If the screen appears too dark to delineate structures, increase the gain setting to brighten the image. Conversely, if the screen is too bright, decrease the gain setting. Vessels should appear as circular structures with a dark or “anechoic” center, indicating blood within the lumen that allows the ultrasound beam to pass through easily (Figure 5).

Figure 5 - increasing the gain setting to brighten the image

Several critical aspects of the target vessel must be assessed during imaging to ensure suitability for cannulation, including vessel type (venous vs. arterial), diameter, depth, patency, and proximity to other structures.

Vessel Assessment: Begin by verifying that the target is a vein. Veins have thinner walls compared to arteries and are compressible. Gentle pressure applied to the vein should cause the walls to collapse inward and meet, confirming its venous nature. Compression also ensures there is no intraluminal obstruction, such as a venous clot (Video 2).

Video 2 – applying pressure to the vessels

Next, assess the vessel’s depth using the depth markers displayed on the ultrasound screen, which typically indicate depth in centimeters. For example, a vessel aligned with the second hash mark from the top of the screen would be located at a depth of 2 cm from the skin surface (Figure 6).

Figure 6 - Measuring the depth of the vessel

Once the depth is measured, determine the vessel diameter, which is essential for selecting the appropriate catheter size for peripheral IV access. Finally, rotate the transducer 90 degrees to visualize the vessel in its long axis, ensuring that the target location is not near a branch point or valve.

Catheter Selection: In peripheral IV access, depth and diameter measurements determine the appropriate catheter size. Peripheral IV catheters vary in diameter (gauge), with smaller gauge numbers indicating larger catheter diameters (e.g., 16G is larger than 22G). A vessel diameter greater than 4 mm (0.4 cm) can accommodate an 18G or smaller catheter without occlusion. 

Figure 7 - Catheters

Catheters also come in various lengths, which affect their stability and suitability for deeper vessels. The depth of the target vessel determines the required catheter length, as longer catheters provide greater stability within the vein [2,3].

Figure 8 - Hypotenuse (needle track), [the image provided by authors]

The needle length required to reach the target vessel can be approximated using the Pythagorean theorem:

a2 + b2 = c2,

where c represents the needle track (hypotenuse. figure 8), a is the vessel depth, and b is the distance from the probe to the needle insertion point. For example, for a vessel 1.2 cm deep with a needle insertion point 1.2 cm distal to the probe, the calculation would be:

1.22 + 1.22 = c2,

resulting in c = 1.69 cm. A simpler method is to multiply the vessel depth by 1.4 (e.g., 1.2 cm × 1.4 = 1.68 cm). To ensure catheter stability within the vein, use the following formula to estimate the necessary catheter length:

Catheter Length = (Vein Depth × 1.4) × 3

This formula accounts for 1/3 of the catheter length reaching the vessel and 2/3 residing within the vein lumen. For example, a 6 cm catheter should not be used for vessels deeper than 1.6 cm.

For peripheral venous access, the following characteristics define an appropriate target vessel for US-guided peripheral IV access:

  • Easily compressible with light pressure applied using the ultrasound probe.
  • Follows a straight path as it travels proximally.
  • Lacks valves that would impede the passage of the cannula or flow after insertion.
  • Diameter greater than 0.4 cm.
  • Close to the skin surface, at a depth of less than 1.6 cm.

For central venous access, the same general principles apply. Regarding vessel diameter and depth, large-diameter vessels that are as superficial as possible are optimal. However, given the nature of these vessels in adult patients and the equipment used for central venous access, the exact parameters regarding diameter and depth mentioned for peripheral vein characteristics do not rigidly apply. Large-diameter vessels such as the internal jugular veins, subclavian veins, and femoral veins are preferred, and access should ideally be attempted at the point where the vessel is located as superficially as possible [4].

Regardless of whether peripheral or central IV access is utilized, the procedure under ultrasound guidance involves dynamically guiding the needle tip to prevent complications. Dynamic cannulation can be performed using either a transverse, out-of-plane approach or a longitudinal, in-plane approach. The transverse view, also known as the out-of-plane approach, is the most commonly used and involves visualizing the needle as a hyperechoic (bright) dot on the ultrasound screen. In contrast, the in-plane approach allows direct visualization of the entire needle length in a long-axis plane but is more challenging for novices, as the needle must remain within the ultrasound beam.

As the metallic needle within the catheter is hyperechoic, it appears as a white dot in the transverse plane and a long hyperechoic line in the longitudinal plane (Figure 9).

Figure 9 - the metallic needle within the catheter is hyperechoic, it appears as a white dot in the transverse plane and a long hyperechoic line in the longitudinal plane

In the transverse plane, it is critical to track the needle tip as it pierces the ultrasound beam, as the appearance of the needle looks the same regardless of its position along the beam. This tracking is achieved by alternating movements of the transducer and the needle. By “leading” with the transducer, then advancing the needle, the tip can be visualized first. Once the needle is seen, advancement should pause, and the transducer should slide slightly proximal up the vein where the needle is no longer visible, after which the needle can be advanced again (Figure 10). This alternating movement allows visualization of the tip as it progresses through the soft tissue and can be repeated until the vein is cannulated (Video 3).

Figure 10a - Walking down the vein: This sequence illustrates the process of "walking down the vein" as observed on an ultrasound. From left to right: the needle initially appears, then disappears, and later re-emerges deeper within the soft tissue before vanishing again. This phenomenon occurs due to the probe moving away, and when the needle reappears, it simply aligns with the ultrasound beam. Note that in real-time, the needle’s positional changes are more gradual than shown here; the figure above is a simplified representation of the concept (refer to the accompanying video for details). [The image was provided by authors].

Video 3 – Walking down the vein

Once the needle is visualized within the vein, the transducer can be rotated to ensure that the needle tip is within the vein lumen and has not pierced the back wall of the vessel. This visualization also allows for redirection of the needle before catheter insertion, ensuring smooth placement when the catheter is advanced off the needle (Video 4). For central venous catheters, a guidewire is inserted after confirming the needle’s position within the vein lumen.

Video 4 – provided by authors

After successfully inserting the IV line, blood return should be verified, and the catheter should be secured in place. As a final confirmation, flush the line. For peripheral IVs, place the ultrasound transducer proximally from the IV site, flush the line, and observe for turbulence or a “glitter artifact” caused by fluid rushing through the vein (Video 5).

Video 5 – provided by authors

This step confirms successful IV cannulation and can also assist in troubleshooting. If the “glitter” does not appear within the vein, the IV catheter is outside the vessel and unusable. For central lines, this confirmation can be performed by visualizing the “glitter” artifact in the right ventricle using the subxiphoid plane within three seconds of flushing the distal port of the line (Video 6).

Video 6 – Glitter Artifact [the video was provided by authors]

Step by Step Guide for US-Guided Peripheral IV Access [3,8]

  1. Verify the identity of the patient who is to undergo IV access and explain the procedure to the patient/healthcare surrogate (when possible).
  2. Position the ultrasound machine on the same side of the patient as the operator.
  3. Don examination gloves.
  4. Clean the ultrasound probe with institution-approved disinfectant.
  5. Remove gloves and replace with clean gloves.
  6. Position stool/chair and adjust the ultrasound machine for the best screen viewing when obtaining access.
  7. Apply an elastic tourniquet proximal to the site to be screened for potential access sites.
  8. Apply ultrasound gel to the target area and orient the probe perpendicularly to the patient’s extremity to obtain a transverse/short-axis view of the target vessels.
  9. Orient the probe indicator to match the orientation displayed on the ultrasound screen, with both conventionally indicating the patient’s right side (Figure 3a).
  10. Assess potential veins for appropriate depth, diameter, and patency.
  11. Veins should:
    • Be greater than or equal to 0.4 cm in diameter for an 18G catheter.
    • Be less than 1.6 cm in depth for a 6 cm length catheter.
    • Be easily compressible without evidence of clots, valves, or other obstructions to blood flow.
  12. Clean off ultrasound gel and release the tourniquet.
  13. Clean the selected site with skin disinfectant and allow it to air dry per manufacturer instructions.
  14. Set up supplies (prepare IV catheter, securement device, port, flush, and dressing).
  15. Cover the ultrasound probe with an occlusive cover.
  16. Avoid touching the head of the probe or the portion of the cover that will contact the patient’s skin.
  17. Reapply the tourniquet and ensure the patient’s arm remains in the appropriate position.
  18. Apply sterile ultrasound gel to the site.
  19. Do not touch the site with gloves or allow uncleaned materials/surfaces to come into contact with the site.
  20. If the site is potentially contaminated, remove the gel and clean the site again before attempting vascular access.
  21. Position the probe and locate the target vein again.
  22. At approximately a 45-degree angle, puncture the skin underneath the ultrasound probe head, observing on ultrasound for the needle tip in the subcutaneous tissue.
  23. Once the needle tip has been visualized, slide the probe proximally away from the needle tip.
  24. Once the needle tip is no longer visualized on ultrasound, carefully advance the needle in 1-2 mm increments until the needle tip returns into view on ultrasound.
  25. Repeat this alternating probe-needle advance until the needle has been advanced into the target vessel (Video 3).
  26. Decrease the angle of the needle as needed to continue advancing the needle in the alternating probe-needle manner within the vessel, keeping the needle tip in the center of the vessel lumen.
  27. Once the needle has been advanced several millimeters into the target vessel, anchor the hand holding the needle to ensure it does not advance further and lay down the ultrasound probe.
  28. Keeping the needle still, advance the catheter over the needle into the vessel.
  29. Once the catheter has been advanced, keep the catheter in place with the hand which advanced the catheter and use the other hand to carefully remove the needle.
  30. Ensure the safety needle capping mechanism on the needle has activated (if automatic upon needle removal from catheter) or activate the safety needle capping mechanism (if not designed to engage automatically) and dispose of the needle into a designated sharps container.
  31. Attach extension tubing and port to the catheter hub (some catheters come with the extension tubing and hub pre-attached).
  32. Clean any remaining ultrasound gel or blood from the access site and secure the catheter with an occlusive dressing.
  33. Attach a saline flush to the hub.
  34. If any air remains in the catheter extension tubing (if applicable), be sure to aspirate any air prior to attempting to flush the line.
  35. Retrieve the ultrasound probe and place it along the vessel proximal on the extremity to the catheter.
  36. After confirming the absence of air in the catheter and extension tubing, flush several cc’s of crystalloid solution through the catheter.
  37. If the catheter is in the correct position and functioning correctly, a “glitter” artifact effect should be visualized within several seconds of pushing the fluid through the catheter (Video 6).
  38. Dispose of supplies in appropriate containers and clean the ultrasound probe with disinfectant wipes.
  39. Remove gloves and wash hands.
  40. Document the access site in the patient’s chart, including site location, catheter gauge, time placed, and operator placing the line.
  41. Ensure you and your team frequently assess the site and extremity for evidence of extravasation, hematoma formation, or other complications.

Step by Step Guide for US-Guided Central Venous Access [4,9]

  1. Verify the identity of the patient who is to undergo IV access and explain the procedure to the patient/healthcare surrogate (when possible).
  2. Position the ultrasound machine on the opposite side of the patient as the operator in the operator’s line of sight.
  3. Don examination gloves.
  4. Clean the ultrasound probe with institution-approved disinfectant.
  5. Remove gloves and replace with clean gloves.
  6. Apply ultrasound gel to the target area and orient the probe perpendicularly to the patient’s extremity to obtain a transverse/short-axis view of the target vessels.
  7. Orient the probe indicator to match the orientation displayed on the ultrasound screen, with both conventionally indicating the patient’s right side (Figure 3a).
  8. Assess potential veins for appropriate depth, diameter, and patency:
  9. Veins should:
    • Be greater than or equal to 0.4 cm in diameter for an 18G catheter.
    • Be less than 1.6 cm in depth for a 6 cm length catheter.
    • Be easily compressible without evidence of clots, valves, or other obstructions to blood flow.
  10. Clean off ultrasound gel.
  11. Clean the selected site with skin disinfectant and allow it to air dry per manufacturer instructions.
  12. Open the central venous catheter kit (or, if unavailable, establish a sterile field upon which to place sterile equipment).
  13. Don eye protection, face mask, and bouffant/scrub cap.
  14. Don a sterile gown and gloves.
  15. Drape the patient in a sterile fashion.
  16. Place the dominant hand within a sterile ultrasound probe cover (if rubber bands to secure the sheath to the probe are included, consider applying rubber bands around the thumb of the dominant hand before placing the hand within the sheath).
  17. Apply sterile gel to the inside of the sheath, which will contact the ultrasound probe head.
  18. Have an assistant pass the linear probe and grab the probe head with the dominant hand surrounded by the ultrasound probe sheath.
  19. Carefully extend the sheath around the probe. Once able, ask an assistant to grab the open end of the probe sheath and pull it toward them along the probe’s wire until it is well away from the sterile field. The assistant can gently release the probe wire now covered in the sheath, being careful not to let the contaminated end of the probe cover touch the sterile field.
  20. Apply the rubber bands (if applicable) to the head of the probe and smooth any air bubbles or irregularities which may have formed along the transducer surface while inserting the probe.
  21. Draw up several cc’s of local anesthetic into a syringe.
  22. Apply sterile ultrasound gel to the target site and confirm there has been no change in positioning of the target vessel during setup.
  23. Inject the local anesthetic into the skin and along the track of the needle to the target vessel, being sure to aspirate before each injection.
  24. It is recommended that the injection of the local anesthetic be performed under active ultrasound guidance to minimize the chance of accidental injection into the vessel and to confirm the anesthetic is applied along the intended tract of the needle.
  25. Ensure that air bubbles have been removed from the local anesthetic solution prior to injection, as these air bubbles will distort visualization of the target vessel area due to scattering of the ultrasound beam as it comes into contact with air.
  26. While the local anesthetic takes effect, flush the lumens of the catheter with saline to prevent the introduction of air into the patient’s vasculature and test that the guidewire feeds smoothly and is free of kinks or defects.
  27. With the introducer needle at an approximately 45-degree angle, puncture the skin underneath the ultrasound probe head, observing on ultrasound for the needle tip in the subcutaneous tissue.
  28. Once the needle tip has been visualized, slide the probe proximally away from the needle tip.
  29. Once the needle tip is no longer visualized on ultrasound, carefully advance the needle in 1-2 mm increments until the needle tip returns into view on ultrasound (Figure 8).
  30. Repeat this alternating probe-needle advance until the needle has been advanced into the target vessel, pulling back on the needle plunger to aspirate blood upon entry into the vessel.
  31. Decrease the angle of the needle as needed to continue advancing the needle in the alternating probe-needle manner within the vessel, keeping the needle tip in the center of the vessel lumen.
  32. Once the needle has been advanced several millimeters into the target vessel, anchor the hand holding the needle to ensure it does not advance further and lay down the ultrasound probe.
  33. Keeping the needle still, lay down the ultrasound probe, remove the syringe from the needle, and retrieve the guidewire.
  34. Advance the guidewire through the introducer needle approximately 20 cm, ensuring that it passes freely without resistance. If resistance is encountered, stop advancing immediately and assess the situation.
  35. Keeping one hand on the guidewire at all times, withdraw the introducer needle over the guidewire and place it in a sharps disposal device or bin.
  36. Confirm that the guidewire is in the target vessel using ultrasound to visualize the guidewire in the vessel in long-axis (Figure 9).
  37. Place gauze nearby the guidewire insertion site for use in the upcoming step.
  38. Place the dilator over the guidewire and advance it toward the skin, stopping several centimeters above the skin.
  39. Using the scalpel, make a small linear incision with the blade directed away from the guidewire and the patient. Consider placing gauze over the site after the incision to minimize bleeding.
  40. Using the dominant hand, insert the dilator to the approximate depth of the vessel visualized on ultrasound, using the other hand to hold the guidewire.
  41. It is recommended to use a twisting motion while advancing the dilator with the hand gripping the dilator just above the patient’s skin.
  42. Ensure that the guidewire remains stationary during dilatory insertion.
  43. Remove the dilator over the guidewire and thread the central venous catheter over the guidewire.
  44. Advance the catheter into the vessel over the guidewire while keeping one hand on the guidewire at all times.
  45. The guidewire should emerge from the distal port of the catheter (typically marked with a brown hub and located in the center of the available ports).
  46. Once the catheter has been placed at the appropriate depth into the target vessel, aspirate blood using a syringe from all ports to ensure patency.
  47. Flush all ports with saline to minimize the chance of clotting.
  48. Use the needle driver and suture to secure the line in place.
  49. Clean the site once more and apply an institution-approved antimicrobial dressing.
  50. If the line was placed in an internal jugular or subclavian vein site, obtain a post-procedural chest radiograph to confirm appropriate placement and assess for complications (e.g., pneumothorax).
Figure 9 - Guide-wire in the vessel - long axis view

Complications

Ultrasound-guided venous access, while generally safer than traditional landmark techniques, still carries potential complications, both for peripheral and central line placement.

Complications of US-Guided Peripheral IV Access [1-3,8]

Infiltration/Extravasation: This is a common complication where IV fluid or medication leaks into the surrounding tissue instead of flowing into the vein. It is a leading cause of catheter failure and may occur more frequently with deep brachial veins compared to other antecubital veins. Using a longer catheter can help minimize the risk of infiltration.

Catheter Dislodgement: Catheter dislodgement occurs when the catheter moves out of the vein, leading to loss of venous access and potential extravasation. This complication is more common with deep veins compared to superficial veins. To reduce the risk, it is essential to ensure that a sufficient length of the catheter is properly positioned within the vessel.

Thrombophlebitis: Thrombophlebitis refers to the inflammation of the vein, which may occur during or after IV placement.

Infection: Although studies have shown no increased infection rates with ultrasound guidance compared to traditional methods, the risk of infection remains. Using sterile gel and adhering to proper cleaning techniques can significantly reduce this risk.

Damage to Adjacent Structures: There is a risk of damaging nearby structures, such as arteries and nerves, during peripheral IV placement. This risk is heightened when using deep veins, which are often located closer to these critical structures.

Posterior Vessel Wall Puncture: The short-axis technique, commonly used during ultrasound-guided IV access, has been associated with a higher risk of puncturing the posterior (back) wall of the vessel.

Hematoma: Bleeding and hematoma formation can occur as a result of vein trauma during catheter placement.

Premature Catheter Failure (PCF): Premature catheter failure occurs when the catheter fails within 24 hours of placement. Studies suggest that PCF rates are higher in ultrasound-guided cannulations compared to traditional methods. Common causes include infiltration, dislodgement, and thrombophlebitis.

Complications of Ultrasound-Guided Central Venous Catheter (CVC) Access [4,9,10]

Arterial Puncture/Cannulation: Accidental puncture or cannulation of an artery, such as the carotid artery during internal jugular vein access, is a serious complication. This risk can be mitigated by using real-time ultrasound guidance and ensuring careful visualization of surrounding structures.

Hematoma: Bleeding and hematoma formation are potential complications during central venous catheter placement, especially if there is accidental puncture of surrounding tissues.

Pneumothorax: A collapsed lung (pneumothorax) is a known complication, particularly during subclavian vein access. Ensuring proper technique and real-time imaging can help reduce this risk.

Hemothorax: Bleeding into the pleural space (hemothorax) may occur during central venous access, especially if there is inadvertent damage to vascular structures near the pleural cavity.

Infection: Catheter-related bloodstream infections are a significant risk associated with central lines. Adherence to strict aseptic technique, including the use of sterile drapes, gloves, and probe covers, is essential to minimize this risk.

Thrombosis: Deep vein thrombosis and catheter-related bloodstream infections can occur as a result of CVC placement. Proper placement, routine monitoring, and prompt intervention are critical in reducing this risk.

Nerve Injury: There is a risk of nerve damage, such as brachial plexus injury, during internal jugular vein catheterization. Careful visualization of anatomical landmarks using ultrasound is critical to avoid this complication.

Catheter Malposition: The catheter may be unintentionally placed in an incorrect location, leading to functional and clinical complications. Real-time imaging during and after placement can ensure proper positioning of the catheter.

Air embolism: It is a rare but serious complication associated with both peripheral and central vein catheterization, which can cause significant neurological deficits and seizures if not promptly diagnosed and treated. The pathophysiology involves air entering the venous system due to a pressure gradient between the atmosphere and the veins, which can occur during catheter insertion, maintenance, or removal. The risk of air embolism is heightened by improper patient positioning. In cases of massive air embolism, immediate interventions such as resuscitation, positioning the patient in the left lateral decubitus and Trendelenburg position, and using hyperbaric oxygen therapy or extracorporeal membrane oxygenation can be life-saving.

Hints and Pitfalls

Universal safety precautions are critical for every procedure. This includes the consistent use of personal protective equipment (PPE) and cleaning all equipment before and after use. These practices are essential to protect both the operator and the patient from harm, including the risk of infections or cross-contamination.

Preparation is paramount to ensuring procedural success and minimizing complications. Proper assessment of the target vessel, including its depth, diameter, and patency, along with setting up the necessary equipment in advance, significantly increases the chances of success during cannulation. Needle tip visualization is also crucial throughout the procedure to prevent iatrogenic injuries caused by inadvertently advancing the needle tip into non-target structures near the vessel.

If a cannulation attempt fails or if the intravenous (IV) line fails due to infiltration, subsequent attempts should ideally be made at a different site to avoid cumulative damage to the same area. If a new site cannot be used, attempts should occur proximal to the initial site.

Strategies to Reduce Complications [1-3, 7-10]

Adequate training is a cornerstone of safe and successful ultrasound-guided venous access. Providers must be proficient in real-time ultrasound guidance techniques, which allow precise needle advancement and proper placement. Additionally, sterile technique is essential during all stages of the procedure, including the use of sterile gel and probe covers to minimize infection risk.

Choosing the appropriate vein for cannulation is another key strategy to reduce complications. This decision should be based on careful vein selection, including evaluating its accessibility and suitability for the intended catheter size. Proper catheter length and size selection are equally important, with tools like the Pythagorean theorem aiding in determining the optimal catheter length for stable placement within the vessel.

Visualization of the needle tip during insertion is vital to avoid injury to surrounding structures. The long-axis approach can provide continuous visualization of the needle tip, ensuring accurate placement within the vessel lumen. After catheter placement, ultrasound can confirm the catheter’s position and patency, reducing the risk of complications such as malposition or infiltration.

Post-procedural monitoring is just as important as the procedure itself. Regular assessment of the insertion site is necessary to detect early signs of infection, thrombophlebitis, or other complications, allowing for timely intervention if needed.

Special Patient Groups

Pediatrics

US-guided venous access in pediatric patients has been shown to significantly enhance the success rates and reduce complications associated with vascular access procedures. A retrospective analysis of 1028 US-guided central vascular access procedures in children demonstrated a high success rate of 97.2%, with the left brachiocephalic vein showing a higher success rate than the right [11]. The integration of ultrasound guidance in pediatric venous access procedures is associated with improved outcomes, emphasizing its role as a preferred method in clinical practice.

Geriatrics

US-guided venous access in geriatric patients has been shown to be a highly effective and safe method for catheter placement. The use of ultrasound guidance significantly reduces failure (success rate of 96.36%) and complication rates (7.27%) [12]. US-guided peripherally inserted central catheter insertion in elderly patients also reported high success rate, with minimal complications [13]. The use of ultrasound guidance for internal jugular vein catheterization further supports its efficacy in reducing failure and complication rates for central venous port placement [14]. Overall, the integration of ultrasound guidance in venous access procedures for geriatric patients enhances safety, reliability, and patient outcomes, making it a valuable tool in the management of this vulnerable population [12-14].

Pregnant patients

US-guided venous access provides significant benefits for pregnant patients, particularly by reducing complications and improving procedural success. Real-time ultrasonographic imaging enables clear visualization of target vessels, which is especially critical in cases of challenging anatomy during pregnancy [15]. This approach aligns with the growing adoption of point-of-care ultrasound (POCUS) to enhance success rates in both peripheral and central venous catheterization. By improving patient safety and minimizing complications, ultrasound guidance has become an essential tool for optimizing venous access procedures and ensuring safer care for pregnant patients [16].

Authors

Picture of Zackary Funk

Zackary Funk

Picture of Petra Duran-Gehring

Petra Duran-Gehring

Petra Duran-Gehring M.D., graduated from medical school at LSU Health Sciences Center in New Orleans, and completed her residency in emergency medicine at the University of Florida College of Medicine – Jacksonville. She achieved certification through the American Registry of Diagnostic Medical Sonographers and founded the emergency ultrasound program for the department of emergency Medicine at UFCOMJ. She is a nationally recognized leader in emergency ultrasound education and research, including serving as co-director of the ACEP Ultrasound Management Course, and director for the SEMPA Ultrasound Course. She has lectured throughout the country, and has received numerous teaching awards. When not teaching ultrasound, she loves spending time with her husband and three young sons.

Listen to the chapter

References

  1. Duran-Gehring P. Ultrasound-Guided IV Access. The Essential Emergency Ultrasound Course; 2019. Accessed August 5, 2023.
  2. Duran-Gehring P, Bryant L, Reynolds JA, Aldridge P, Kalynych CJ, Guirgis FW. Ultrasound-Guided Peripheral Intravenous Catheter Training Results in Physician-Level Success for Emergency Department Technicians. J Ultrasound Med. 2016;35(11):2343-2352. doi:10.7863/ultra.15.11059
  3. Gottlieb M, Sundaram T, Holladay D, Nakitende D. Ultrasound-Guided Peripheral Intravenous Line Placement: A Narrative Review of Evidence-based Best Practices. West J Emerg Med. 2017;18(6):1047-1054. doi:10.5811/westjem.2017.7.34610
  4. Leung J, Duffy M, Finckh A. Real-time ultrasonographically-guided internal jugular vein catheterization in the emergency department increases success rates and reduces complications: a randomized, prospective study. Ann Emerg Med. 2006;48(5):540-547. doi:10.1016/j.annemergmed.2006.01.011
  5. Jacobson AF, Winslow EH. Variables influencing intravenous catheter insertion difficulty and failure: an analysis of 339 intravenous catheter insertions. Heart Lung. 2005;34(5):345-359. doi:10.1016/j.hrtlng.2005.04.002
  6. Au AK, Rotte MJ, Grzybowski RJ, Ku BS, Fields JM. Decrease in central venous catheter placement due to use of ultrasound guidance for peripheral intravenous catheters. Am J Emerg Med. 2012;30(9):1950-1954. doi:10.1016/j.ajem.2012.04.016
  7. Shokoohi H, Armstrong P, Tansek R. Emergency department ultrasound probe infection control: challenges and solutions. Open Access Emerg Med. 2015;7:1-9. Published 2015 Jan 5. doi:10.2147/OAEM.S50360
  8. Blanco P. Ultrasound-guided peripheral venous cannulation in critically ill patients: a practical guideline. Ultrasound J. 2019;11(1):27. Published 2019 Oct 17. doi:10.1186/s13089-019-0144-5
  9. Saugel B, Scheeren TWL, Teboul JL. Ultrasound-guided central venous catheter placement: a structured review and recommendations for clinical practice. Crit Care. 2017;21(1):225. Published 2017 Aug 28. doi:10.1186/s13054-017-1814-y
  10. Parienti JJ, Mongardon N, Mégarbane B, et al. Intravascular Complications of Central Venous Catheterization by Insertion Site. N Engl J Med. 2015;373(13):1220-1229. doi:10.1056/NEJMoa1500964
  11. D’Alessandro P, Siffredi JI, Redondo Pertuz E, et al. Retrospective analysis of 1028 ultrasound-guided central vascular access in neonates and children. J Vasc Access. Published online September 26, 2024. Doi:10.1177/11297298241278385
  12. Sun X, Zhang Y, Yang C, et al. Ultrasound-guided totally implantable venous access device through the right innominate vein in older patients is safe and reliable. Geriatr Gerontol Int. 2019;19(3):218-221. doi:10.1111/ggi.13611
  13. Nakano Y, Kondo T, Murohara T, Yamauchi K. Option of Using Peripherally Inserted Central Catheters in Elderly Patients With Dementia: An Observational Study. Gerontol Geriatr Med. 2020;6:2333721420906922. Published 2020 Feb 18. doi:10.1177/2333721420906922
  14. Canfora A, Mauriello C, Ferronetti A, et al. Efficacy and safety of ultrasound-guided placement of central venous port systems via the right internal jugular vein in elderly oncologic patients: our single-center experience and protocol. Aging Clin Exp Res. 2017;29(Suppl 1):127-130. doi:10.1007/s40520-016-0680-9

Reviewed and Edited By

Picture of Arif Alper Cevik, MD, FEMAT, FIFEM

Arif Alper Cevik, MD, FEMAT, FIFEM

Prof Cevik is an Emergency Medicine academician at United Arab Emirates University, interested in international emergency medicine, emergency medicine education, medical education, point of care ultrasound and trauma. He is the founder and director of the International Emergency Medicine Education Project – iem-student.org, chair of the International Federation for Emergency Medicine (IFEM) core curriculum and education committee and board member of the Asian Society for Emergency Medicine and Emirati Board of Emergency Medicine.

Chest Pain (2024)

~ iEM Education Project Team ~ Leave a comment

by Khaled Alaboud Alkheder & Muneer Al Marzooqi

Authors
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You Have A New Patient!

A 67-year-old woman presents to the ED with acute chest pain. The pain is sharp and stabbing in nature. She feels nauseated and short of breath. The patient has a history of hypertension, type 1 diabetes mellitus, medullary thyroid cancer, coronary artery disease, and gastroesophageal reflux disease. She smoked half a pack of cigarettes daily for 19 years but quit 18 years ago. Her current medications include Lisinopril, Insulin Glargine, Insulin Aspart, Sertraline, Aspirin, and Ranitidine.

The image was produced by using ideogram 2.0.

She appears anxious and diaphoretic. Her temperature is 37.2°C, pulse is 62/min, respirations are 19/min, and blood pressure is 142/81 mmHg. The lungs are clear to auscultation. The chest wall and abdomen are non-tender. There is 5/5 strength in all extremities. The remainder of the examination shows no abnormalities.

How would you proceed, and what is the next step in management?

What Do You Need To Know?

Chest pain in the emergency department is reported to be the second most common complaint, comprising approximately 5% of all emergency department visits. It can indicate various underlying causes, and patients present with many signs and symptoms. The potential causes of chest pain include diseases affecting the heart, aorta, lungs, esophagus, stomach, mediastinum, pleura, and abdominal viscera.

Patients usually describe visceral pain as a squeezing, pressure-like, or dull type of pain. If the pain is visceral, it may also refer to other locations due to the nerves coursing through somatic nerve fibers as they reach the spinal cord. For example, ischemic heart pain may refer to the left or right shoulder, jaw, or left arm.

Clinicians in the ED focus on promptly identifying and ruling out life-threatening causes of chest pain. Patients with serious causes of chest pain may not exhibit any vital sign or physical examination abnormalities and may appear healthy [1,2].

Initial Assessment and Stabilization (ABCDE Approach)

The ABCDE approach is universally recognized as the safest and most efficient method for the initial assessment of patients in the Emergency Department (ED), particularly those presenting with chest pain [3]. This systematic approach ensures rapid identification and management of life-threatening conditions. It prioritizes the immediate stabilization of the patient while facilitating a structured evaluation process.

A – Airway: The first step involves assessing the airway for any signs of obstruction. Key indicators include the patient’s ability to speak without distress and the presence of paradoxical chest movements. Obstructions may result from conditions such as tongue swelling, lip swelling, or other factors impeding spontaneous breathing. Ensuring a patent airway is critical, as it serves as the foundation for effective oxygenation and ventilation.

B – Breathing: Next, the breathing assessment evaluates respiratory effectiveness by observing the patient’s respiratory rate (normal range: 10-20 breaths per minute), inspecting for signs of respiratory distress, and auscultating lung sounds. Findings such as basal crackles may indicate pulmonary edema, diminished breath sounds could suggest pneumothorax or pleural effusion. Each of these conditions requires prompt recognition and intervention.

C – Circulation: The circulation step focuses on identifying signs of cardiovascular compromise or shock. Clinical signs include abnormal extremity coloration (blue, pale, pink, or mottled), prolonged capillary refill time (normal is ≤2 seconds), and abnormal heart rates. Auscultation of the heart should confirm normal S1 and S2 sounds without murmurs or gallops. These findings guide the clinician in diagnosing conditions such as hypoperfusion or cardiac dysfunction. Muffled heart sounds may point toward pericardial tamponade. 

D – Disability: Assessment of the patient’s neurological status is crucial, including evaluating their level of alertness, Glasgow Coma Scale (GCS) score, and glucose levels. Any abnormalities here could indicate underlying conditions such as hypoglycemia, traumatic brain injury, or other causes of altered mental status.

E – Exposure: The final step involves fully exposing the patient to detect visible signs such as rashes, discoloration, or gross abnormalities. This step ensures that no critical findings, such as trauma or skin infections, are overlooked.

Once the primary assessment is complete, interventions should focus on managing hemodynamic instability, such as shock or hypertension. Simultaneously, secondary assessments and investigations are initiated, including obtaining IV access, performing a 12-lead ECG, and ordering relevant diagnostic tests to confirm the underlying cause of the presentation.

Medical History

When assessing a patient presenting with chest pain in the Emergency Department (ED), obtaining a thorough history is critical after ensuring the patient’s stability. Key aspects of the history should include [3,4]:

  • Onset of Pain: Determining whether the pain started abruptly or developed gradually provides valuable diagnostic clues.
  • Site of Pain: The location of the pain (e.g., substernal, localized, diffuse, chest wall, or back) can guide the identification of the underlying cause.
  • Character of Pain: Descriptions such as sharp, squeezing, or pleuritic help differentiate between cardiac, pulmonary, and musculoskeletal etiologies.
  • Radiation: Pain radiating to areas like the jaw, back, shoulder, or arm can indicate cardiac involvement.
  • Associated Symptoms: Symptoms such as diaphoresis, palpitations, dyspnea, nausea, or vomiting are important to document.
  • Timing: The pattern of the pain, whether constant or episodic, its duration, and the time of onset can help in distinguishing between various causes.
  • Exacerbating/Relieving Factors: Identifying activities or factors that provoke or alleviate the pain aids in narrowing down the diagnosis.

Pain Descriptions and Differential Diagnosis: The nature of the chest pain provides critical diagnostic insights:

  • Cardiac Origin: Pain described as “squeezing,” “crushing,” or “pressure-like” suggests cardiac ischemia or acute coronary syndrome (ACS). Pain during exertion is typical of stable angina, whereas progressive pain at rest suggests unstable angina or myocardial infarction (MI).
  • Aortic Dissection: “Tearing” pain radiating to the back is a hallmark of aortic dissection.
  • Pulmonary or Musculoskeletal Causes: “Sharp” or “stabbing” pain is often associated with pulmonary embolism, pneumothorax, or musculoskeletal disorders.
  • Gastrointestinal Causes: “Burning” or “indigestion-like” pain may originate from the gastrointestinal tract but could also signify visceral chest pain. Pain triggered by meals is more likely gastrointestinal in origin.
  • Acute Conditions: Sudden onset pain suggests conditions like aortic dissection, pulmonary embolism, or pneumothorax.

Medical Background and Risk Factors: A comprehensive medical history is essential to assess the risk for specific conditions:

  • Risk Factors for Acute Coronary Syndrome (ACS):
    • Male sex
    • Age over 55 years
    • Family history of coronary artery disease
    • Diabetes mellitus
    • Hypercholesterolemia
    • Hypertension
    • Tobacco use
  • Risk Factors for Pulmonary Embolism: Patients are at an increased risk if they have:
    • Prolonged immobilization (e.g., long-distance travel)
    • Recent surgery, especially orthopedic procedures lasting over 30 minutes
    • Central venous catheterization
    • Trauma
    • Pregnancy
    • Cancer
    • Lung or chronic heart disease
    • A personal or family history of hypercoagulability
    • Use of hormonal contraceptives or chemotherapeutic agents that increase estrogen and progestin levels

This detailed and systematic approach to history-taking allows for accurate and timely diagnosis, ensuring that critical conditions are addressed without delay.

Physical Examination

After obtaining a detailed history, a focused physical examination is crucial to identify any signs that may guide the clinician toward an accurate diagnosis. This examination combines general and systemic assessments, prioritizing findings that can point to life-threatening conditions [5,6].

General Examination and Vital Signs:

The initial step involves assessing vital signs, which often provide significant diagnostic clues:

  • Hypotension may indicate conditions such as tension pneumothorax, pulmonary embolism (PE), or acute myocardial infarction (MI).
  • Tachycardia is a nonspecific finding but is frequently seen in acute MI, PE, aortic dissection, or tension pneumothorax.
  • Hypoxemia suggests pulmonary conditions such as PE, tension pneumothorax, or simple pneumothorax.
  • Fever can be indicative of inflammatory or infectious processes, including PE, pericarditis, myocarditis, or even extrapulmonary causes like cholecystitis.

Cardiovascular Examination:

A detailed cardiovascular assessment should focus on specific findings that may narrow the differential diagnosis:

  • Significant blood pressure differences between upper extremities are a hallmark of aortic dissection.
  • Pericardial rub is a characteristic sign of pericarditis.
  • Jugular venous distension (JVD) may indicate tension pneumothorax, PE, or pericarditis with effusion.
  • Narrow pulse pressure can be associated with pericarditis with effusion, reflecting compromised cardiac output.
  • Pulsus paradoxus, an exaggerated drop in systolic blood pressure during inspiration, is a critical finding in cardiac tamponade and constrictive pericarditis.

Pulmonary Examination:

The pulmonary evaluation should focus on auscultation and observation:

  • Unilateral diminished or absent breath sounds point to tension pneumothorax or simple pneumothorax.
  • Pleural rub, a coarse grating sound, may be heard in PE, indicating pleural irritation.
  • Basal crackles (rales), particularly when bilateral, are often associated with acute MI or pulmonary edema, reflecting fluid overload or cardiac dysfunction.

Integration of Findings:

These physical examination findings must be interpreted in the context of the patient’s history and associated risk factors. For example:

  • A patient presenting with hypoxemia, tachycardia, and JVD warrants an immediate evaluation for PE.
  • Tension pneumothorax should be suspected in cases with hypotension, unilateral absent breath sounds, and JVD.
  • Signs of basal crackles and a pericardial rub may point to a combination of acute MI and pericarditis, necessitating rapid interventions.

By systematically combining history with these focused examination findings, clinicians can efficiently narrow their differential diagnosis and prioritize further investigations and treatments. This structured approach ensures that life-threatening conditions are promptly identified and managed.

When To Ask for Senior Help

Remember that senior residents and attendings supervise you when working in the emergency department. It is important to ask for their help when needed, especially when a patient with chest pain arrives [6]. The following are situations when you need to call for help immediately in a patient with chest pain:

  • Patients clenching their chest with ongoing chest pain and diaphoresis.
  • Chest pain with severe shortness of breath and evidence of pulmonary edema.
  • Chest pain with hypotension.
  • Chest pain with severe bradycardia or tachycardia.
  • Chest pain followed by unresponsiveness.

These examples exhibit life-threatening features of chest pain that can be lethal within minutes. You must call for help, and the team will be assembled to care for the patient and administer lifesaving interventions.

Alternative Diagnoses

Chest pain is a common presentation in the Emergency Department (ED) and requires a systematic and thorough approach to rule out life-threatening conditions. These diagnoses must be prioritized in the differential diagnosis as they carry significant morbidity and mortality if not identified and managed promptly [1,6].

Life-Threatening Diagnoses:

  1. Acute Coronary Syndrome (ACS): ACS encompasses conditions such as unstable angina, non-ST elevation myocardial infarction (NSTEMI), and ST elevation myocardial infarction (STEMI). These result from ischemia due to decreased myocardial oxygen supply, often caused by atherosclerotic plaque rupture. Rapid identification through ECG and biomarkers is critical to initiate timely treatment.

  2. Acute Aortic Dissection: This condition arises when a tear in the intimal layer of the aorta allows blood to flow between the layers, creating a false lumen. Patients often present with severe, tearing chest or back pain and may have a significant difference in blood pressure between the upper extremities. Early diagnosis via imaging such as CT angiography is essential to prevent fatal rupture.

  3. Pulmonary Embolism (PE): PE results from the occlusion of pulmonary arteries by thromboemboli, often originating from deep vein thrombosis (DVT). Symptoms include sudden onset dyspnea, chest pain, and hypoxemia. Clinical suspicion should be high in patients with risk factors like prolonged immobilization, recent surgery, or hypercoagulable states.

  4. Tension Pneumothorax: This is a critical condition where air accumulates in the pleural space under pressure, compressing the lungs and mediastinum. Patients may present with hypotension, respiratory distress, and absent breath sounds on the affected side. Immediate needle decompression is lifesaving.

  5. Pericardial Tamponade: This occurs when fluid accumulates in the pericardial sac, impairing cardiac filling and output. Classic findings include hypotension, jugular venous distension, and muffled heart sounds (Beck’s triad). Pulsus paradoxus is another critical clue. Echocardiography confirms the diagnosis, and pericardiocentesis is the treatment.

  6. Esophageal Rupture with Mediastinitis: Esophageal rupture, also known as Boerhaave syndrome, can lead to mediastinitis due to leakage of gastric contents into the mediastinum. Patients typically present with severe chest pain following vomiting, subcutaneous emphysema, and signs of sepsis. Prompt surgical intervention is required.

Other Diagnoses to Consider:

  1. Simple Pneumothorax: Unlike tension pneumothorax, simple pneumothorax lacks hemodynamic compromise but still requires prompt recognition. Patients may present with pleuritic chest pain and diminished breath sounds on the affected side. Treatment typically involves observation or chest tube placement, depending on severity.

  2. Pericarditis: This inflammatory condition of the pericardium often presents with sharp, pleuritic chest pain that is relieved by sitting up and leaning forward. A pericardial rub is the hallmark auscultatory finding. ECG changes, including diffuse ST elevation, aid in the diagnosis. Most cases are viral and self-limiting, though complications like effusion and tamponade must be monitored.

Acing Diagnostic Testing

To accurately diagnose the cause of chest pain, a combination of bedside tests and advanced investigations are essential. These tests provide critical information that can guide immediate management, particularly in identifying life-threatening conditions [1,2].

Bedside Tests

Electrocardiogram (ECG):

The 12-lead ECG is a cornerstone of chest pain evaluation and must be performed within 10 minutes of the patient’s presentation or EMS arrival. It aids in identifying acute coronary syndromes (ACS), including ST-elevation myocardial infarction (STEMI).

STEMI Criteria:
  • General Criteria: At least 1 mm of ST elevation in two contiguous leads, excluding V2 and V3.
  • Specific Criteria for V2 and V3 ST Elevation:
    • Women: ≥1.5 mm elevation.
    • Men <40 years: ≥2.5 mm elevation.
    • Men ≥40 years: ≥2 mm elevation.
Source: Hernandez JM, Glembocki MM, McCoy MA. Increasing Nursing Knowledge of ST-Elevated Myocardial Infarction Recognition on 12-Lead Electrocardiograms to Improve Patient Outcomes. The Journal of Continuing Education in Nursing. 2019;50(10):475-480. doi:10.3928/00220124-20190917-10
Inferior ST segment elevations with anterior and lateral reciprocal changes. Inferior MI, so the right side of the heart should be evaluated with right side chest leads. V2 ST depression is very prominent, therefore, posterior leads should be applied form V7 to V12 for the left side.
43 years-old patients with left sided chest pain. Courtesy of Khaled Alaboud Alkheder and Muneer Al Marzooqi
Clinical Interpretation of the ECG above:
  • For instance, an ECG from a 43-year-old male presenting with severe left-sided chest pain showed ST elevation in anteroseptal leads (V1-V4) with J point elevation >2 mm and reciprocal ST depression in inferior leads, indicative of an acute anterior STEMI. This finding underscores the importance of identifying patterns such as J point elevation, which marks the transition between the QRS complex and the ST segment.

ECG Limitations and Additional Considerations:

  • While some patients exhibit a classic STEMI pattern, many may present with a normal or non-diagnostic ECG. A normal ECG at admission cannot rule out ACS or other conditions, necessitating further testing if clinical suspicion remains high.
  • If the initial ECG is inconclusive, it should be repeated after a 10-minute interval, especially if chest pain recurs.
  • Additional leads should be utilized when clinical suspicion exists for specific myocardial infarctions:
    • Posterior leads (V7-V9): For suspected posterior MI.
    • Right-sided leads (V3R and V4R): For patients with acute inferior MI, to assess for right ventricular involvement.
  • In suspected pulmonary embolism (PE), the S1Q3T3 pattern (prominent S wave in lead I, Q wave in lead III, and inverted T wave in lead III) may suggest right heart strain, though it is neither sensitive nor specific for PE [5].
S1Q3T3 - Courtesy of Khaled Alaboud Alkheder and Muneer Al Marzooqi
ECG 54-yo male chest pain for the last 3 days. S1 Q3 T3, Tachycardia, minor ST depressions on lateral leads (V5-6)

The ECG is a highly valuable tool for ruling in STEMI or other acute conditions. However, its limitations in ruling out conditions underscore the necessity of adjunct investigations and clinical correlation. For example, repeated ECGs, additional lead placements, and further imaging or lab tests (such as cardiac biomarkers or D-dimer for PE suspicion) ensure comprehensive evaluation and timely intervention.

By systematically incorporating these investigative steps into the diagnostic process, clinicians can optimize patient outcomes and address the underlying etiology of chest pain effectively.

Laboratory Tests

In the assessment of patients presenting with chest pain, laboratory investigations play a crucial role in diagnosing life-threatening conditions such as acute myocardial infarction (AMI) and pulmonary embolism (PE). Among the most valuable tests are cardiac troponins and D-dimer levels, each serving distinct purposes based on clinical suspicion and patient presentation.

Cardiac Troponins:

  • Utility in AMI Diagnosis:
    Cardiac troponins, specifically high-sensitivity troponin I and T, are the preferred laboratory markers for diagnosing AMI. These biomarkers can reliably detect myocardial injury within 3 hours of symptom onset. Their high sensitivity and specificity make them the gold standard in confirming myocardial infarction (MI).

  • Role in Ruling Out MI:
    While cardiac troponins are essential for diagnosing AMI, a single set of negative cardiac enzyme results is insufficient to rule out MI, especially in early presentations. However, in patients presenting with chest pain lasting over 2 hours, a single undetectable troponin T level can help exclude MI in certain cases [1].

  • Detection of Unstable Angina:
    High-sensitivity troponin assays can also detect subtle elevations associated with unstable angina, aiding in the identification of patients at risk for adverse cardiac events. However, serial testing may be required to observe trends and confirm the diagnosis.

D-Dimer:

  • Screening for Pulmonary Embolism (PE):
    D-dimer testing is particularly valuable in patients with suspected PE. In low-risk patients, a negative D-dimer test effectively rules out PE, eliminating the need for further imaging.

  • High-Risk Patients:
    Patients identified as high-risk based on clinical assessment or pretest probability should proceed directly to diagnostic imaging, such as computed tomography pulmonary angiography (CTPA). Similarly, patients with an intermediate or high pretest probability should not rely solely on D-dimer results but instead undergo confirmatory imaging [5].

These laboratory investigations provide critical insights when integrated with clinical findings and other diagnostic tools. For example:

  • In patients presenting with prolonged chest pain and an elevated troponin level, AMI is highly likely, warranting immediate intervention.
  • Conversely, in patients with a low-risk Wells score for PE and a negative D-dimer, further imaging can be safely avoided, reducing unnecessary radiation exposure and costs.

Imaging

In the assessment of chest pain, imaging plays a pivotal role in identifying life-threatening conditions and narrowing the differential diagnosis. A combination of imaging techniques can provide vital insights into both cardiac and non-cardiac causes of chest pain.

Chest X-Ray

  • Role in Emergency Evaluations:
    Chest X-rays are widely used in emergency departments as an initial imaging modality. They are particularly useful for identifying acute and life-threatening conditions, including pericardial effusion, acute aortic dissection, pulmonary embolism (PE), pneumothorax, and pneumonia.

    • Timeliness: In cases of high clinical suspicion, a chest X-ray should be performed and interpreted within 30 minutes to avoid delays in diagnosis and treatment.

  • Limitations:
    While chest X-rays are a valuable starting point, their sensitivity and specificity may be limited for certain conditions, necessitating further imaging in many cases.

Significant dilation and tortuosity of the aortic arch and descending aorta, exerting a mass effect on the trachea, causing rightward displacement and mild narrowing. Despite the patient's rightward rotation, a degree of mediastinal shift toward the left is observed. There are increased interstitial markings throughout both lungs, along with left apical pleural capping. - Source: Hacking C Large thoracic aortic aneurysm. Case study, Radiopaedia.org (Accessed on 31 Dec 2024) https://doi.org/10.53347/rID-73356
Pneumothorax on the left side (courtesy of Mohd Mokhtar and Raja Ahmad)
Ultrasonography

  • Advantages of POCUS:
    Point-of-care ultrasound has become an indispensable tool in emergency settings due to its rapid and dynamic assessment capabilities. It can evaluate both cardiac and non-cardiac causes of chest pain with high accuracy.

  • Cardiac Applications:

    • Detection of pericardial effusion and cardiac tamponade is a primary use of POCUS.

    • Example: A significant pericardial effusion may appear as a fluid collection around the heart, as visualized in Figure 5.

  • Pulmonary Applications:

    • POCUS has a higher sensitivity and specificity than chest X-rays for detecting pleural effusion and pneumothorax.

    • Pneumothorax Findings: The absence of the seashore sign (lung sliding) and the presence of the barcode sign on M-mode ultrasound strongly suggest pneumothorax.

    • Acute Heart Failure Findings: In cases of acute ischemic chest pain, lung B-lines detected on ultrasound indicate pulmonary edema due to heart failure.

Subxiphoid 4 Chambers View. PE = Pericardial Effusion, RV = Right Ventricle, LV = Left Ventricle
CT Pulmonary Angiography (CTPA)

  • Gold Standard for PE Diagnosis:
    CT pulmonary angiography (CTPA) is the imaging modality of choice for diagnosing acute pulmonary embolism (PE). Its high sensitivity and specificity make it invaluable for confirming or excluding PE in patients with high clinical suspicion.

  • Additional Findings:
    Beyond diagnosing PE, CTPA can reveal other significant pathologies, including [3,5]:

    • Pneumonia
    • Pericardial abnormalities
    • Musculoskeletal injuries
Pulmonary Embolism - Bilateral thrombus in main pulmonary arteries

Management

Patients presenting with typical chest pain are at a high risk of having Acute Coronary Syndrome. Empiric and symptomatic treatment is paramount in the ED to help control the situation and alleviate the patient’s pain. A common mnemonic used is (MONA), where patients can be given Morphine, which is an opiate, to help relieve the pain. Oxygen supplementation is recommended, but studies have shown that hyperoxygenation and hyperoxia are harmful and can lead to oxygen radicals; therefore, patients are maintained with oxygen saturation between 94–96% [2,6].

As a sublingual administration, Nitroglycerin is used to overcome coronary vasospasm and helps with vasodilation of the coronary vessels to improve blood flow to the myocardium and relieve ischemic chest pain. Finally, Aspirin, as an antiplatelet agent, is used empirically to prevent further clot formation and is one of the mainstay treatments when Acute Coronary Syndrome is suspected.

Aspirin

Dose: 162 to 325 mg in cases of acute coronary syndrome (ACS).
Frequency: Single dose.
Maximum Dose: 4 grams in 24 hours.
Category in Pregnancy: Category C.
Cautions/Comments: Prior to administration, check for allergies, bleeding disorders, or a history of bleeding gastrointestinal (GI) ulcers, as these conditions contraindicate the use of aspirin.

Nitroglycerin (Sublingual or Puffs)

Dose: For sublingual tablets, 0.4 mg per dose. For metered spray, 400 mcg of nitroglycerin per puff.
Frequency: For sublingual administration, up to 3 doses; for puffs, administer every 5 minutes with no more than 3 sprays in a 15-minute period.
Maximum Dose: Up to 3 doses (sublingual) or sprays (puffs) within a 15-minute period.
Category in Pregnancy: Category C.
Cautions/Comments: Nitroglycerin may cause hypotension, particularly with an upright posture. It is contraindicated in patients using phosphodiesterase inhibitors (e.g., for erectile dysfunction).

Morphine

Dose: 4 to 10 mg.
Frequency: Administer 2.5 to 5 mg every 3-4 hours as needed (PRN) or infused over 4-5 minutes.
Maximum Dose: 0.1 to 0.2 mg/kg.
Category in Pregnancy: Classified as Category CFR (consult further resources for more information).
Cautions/Comments: Monitor patients for respiratory depression. Co-ingestion with alcohol increases the risk of a fatal overdose and should be avoided.

Special Patient Groups

Pediatrics

Chest pain in children presenting to the emergency department can be a challenging clinical scenario, as it often raises concerns about serious underlying conditions, including cardiac issues, although they are relatively rare in this population. The differential diagnosis for pediatric chest pain includes musculoskeletal pain, respiratory conditions, gastrointestinal issues, and, less commonly, cardiac abnormalities such as myocarditis or pericarditis [7]. A thorough history and physical examination are essential to differentiate between these causes, considering factors such as the nature of the pain, associated symptoms, and the child’s medical history [8]. While most cases of chest pain in children are benign, it is crucial for healthcare providers to maintain a high index of suspicion and to utilize appropriate diagnostic tools, such as electrocardiograms and imaging studies, when indicated [9].

Pregnant Patients

Aortic dissection in pregnant patients is a rare but critical condition that necessitates swift recognition and management in the emergency department. Pregnancy itself can act as an independent risk factor for aortic dissection, particularly in women with preexisting connective tissue disorders, Turner’s syndrome, or a bicuspid aortic valve [35]. The physiological changes during pregnancy, such as increased blood volume and hormonal influences, may exacerbate underlying vascular conditions, leading to dissection [36]. Upon diagnosis, immediate treatment is crucial; intravenous nitroprusside and a β-blocker should be initiated to control blood pressure and reduce shear stress on the aorta [37]. Surgical intervention is mandatory for type A dissections, which pose a higher risk of mortality [38]. Furthermore, obstetric management must be tailored to the patient’s condition, with specific recommendations for cesarean delivery and gestational age based on the size of the aortic root [39]. Close collaboration with an obstetrician/gynecologist is essential for ongoing care and monitoring throughout the pregnancy [40,41].

Geriatrics

Older adults often experience less classic symptoms of myocardial infarction, such as chest pressure or pain, and may instead report vague symptoms like fatigue, shortness of breath, or confusion, which can complicate diagnosis [14]. Additionally, the presence of multiple chronic conditions may lead to an increased risk of complications and poorer outcomes [15]. Timely and accurate assessment is critical, as delays in diagnosis can significantly impact morbidity and mortality rates in this population [16]. Therefore, a high index of suspicion and thorough evaluation, including appropriate imaging and laboratory tests, are essential in managing chest pain in geriatric patients effectively [17].

When To Admit This Patient

Disposition decisions for patients presenting with chest pain in the emergency department (ED) are critical for ensuring appropriate care and minimizing the risk of adverse cardiovascular events. According to guidelines established by the American College of Cardiology and the American Heart Association (ACC/AHA), patients exhibiting high-risk features, such as ST-segment elevation on an electrocardiogram (ECG), hemodynamic instability, or signs of heart failure, should generally be admitted to the hospital for further evaluation and management [18]. Additionally, those presenting with intermediate-risk features—such as abnormal ECG readings, elevated cardiac biomarkers like troponin, or a history of coronary artery disease—also warrant hospitalization [19]. Conversely, low-risk patients, characterized by a normal ECG and negative cardiac biomarkers, may be safely discharged based on clinical judgment and validated risk stratification tools [19]. Ultimately, the decision to admit a patient with chest pain hinges on a comprehensive assessment of their symptoms, medical history, and individual risk factors for serious cardiovascular events, ensuring that high-risk patients receive the necessary care while minimizing unnecessary hospitalizations for those at lower risk [20].

Risk Stratification

The HEART Score is a clinical tool used to evaluate the risk of major adverse cardiac events (MACE) in patients presenting with chest pain. It assesses five key components: history, ECG findings, age, risk factors, and troponin levels, with each category assigned a score ranging from 0 to 2 points. The total score determines the level of risk and guides subsequent management.

History is assessed based on clinical suspicion. A highly suspicious history earns 2 points, a moderately suspicious history scores 1 point, and a slightly or non-suspicious history scores 0 points. This subjective component emphasizes the importance of a thorough clinical evaluation.

ECG findings are evaluated next. Significant ST-depression earns 2 points, nonspecific repolarization changes score 1 point, and a normal ECG scores 0 points. This category highlights the significance of electrocardiographic abnormalities in cardiac risk stratification.

Age is another important factor. Patients aged 65 years or older receive 2 points, those aged between 45 and 65 years earn 1 point, and patients 45 years or younger score 0 points, reflecting the age-related risk of cardiac events.

Risk factors are categorized based on their number and severity. Patients with three or more risk factors or a history of coronary artery disease (CAD) receive 2 points. Those with one or two risk factors score 1 point, while individuals with no risk factors score 0 points. Risk factors include diabetes mellitus (DM), hypertension (HTN), hyperlipidemia (HLP), smoking (current or recent), obesity, and a family history of CAD.

Troponin levels are also considered. Levels three or more times the normal limit score 2 points, levels one to three times the normal limit earn 1 point, and normal troponin levels score 0 points. This biomarker is critical in identifying myocardial injury.

The total HEART Score helps categorize patients into low, moderate, or high risk for MACE over the next six weeks. A score of 0-3 corresponds to a 2.5% risk and suggests discharge home. A score of 4-6 indicates a 20.3% risk, warranting clinical observation. Scores of 7-10 reflect a 72.7% risk, prompting early invasive strategies. This systematic approach helps clinicians make evidence-based decisions for managing patients with chest pain.

Each variable is scored from 0 to 2, allowing for a comprehensive assessment of the patient’s risk profile. For instance, the patient’s history is examined for indicators of coronary artery disease (CAD), while the ECG is scrutinized for signs of ischemia, such as ST-segment depression [21]. Age is considered a significant risk factor, as older patients are at higher risk for CAD, and the presence of additional risk factors like hypertension, hyperlipidemia, smoking, and diabetes further elevates this risk [22]. Elevated troponin levels serve as a critical marker for myocardial ischemia or infarction. The total HEART score, ranging from 0 to 10, categorizes patients into different risk levels, guiding management decisions regarding further testing, hospitalization, or early discharge [23]. However, it is essential to use the HEART score in conjunction with clinical judgment, as it should not be the sole determinant in decision-making processes [24].

Revisiting Your Patient

The patient had presented with complaints of chest pain, shortness of breath, diaphoresis, and nausea, raising the suspicion of Acute Coronary Syndrome and possible Myocardial Infarction. This suspicion had been supported by her significant risk factors, which included insulin-dependent diabetes mellitus, hypertension, a 12-pack-year smoking history, and a history of ischemic heart disease.

Initial stabilization measures had been promptly undertaken. The patient had been placed in a monitored bed and connected to a cardiac monitor. The ABCDE approach had been followed, and it had been noted that she was vitally stable. A quick history had been obtained, which revealed a sudden onset of central chest pain, described as sharp and stabbing, accompanied by diaphoresis and nausea. On physical examination, equal air entry had been observed with no wheeze or crackles on chest auscultation. A cardiovascular examination had also been planned.

Based on the initial presentation and clinical findings, a cardiac workup had been deemed necessary. This included ordering Troponin T and I tests, performing a 12-lead ECG, and obtaining a portable chest X-ray to rule out potential complications such as congestive heart failure, pneumonia, or pneumothorax.

Therapeutic interventions had been initiated promptly. The patient had been started on supplemental oxygen via a nasal cannula or face mask. Analgesics had been administered while ensuring no contraindications or allergies were present. These included IV paracetamol, IV opioids such as morphine or fentanyl, and sublingual nitroglycerin, either as a puff or tablet. These measures had been aimed at relieving the patient’s symptoms and stabilizing her condition.

Authors

Picture of Khaled Alaboud Alkheder

Khaled Alaboud Alkheder

Tawam Hospital Emergency Medicine Residency Program, United Arab Emirates

Picture of Muneer Abdulla Al Marzooqi

Muneer Abdulla Al Marzooqi

Dr. Muneer is a Consultant Emergency Medicine Physician from the UAE. He completed his EM residency at Tawam Hospital in 2017 and has served as an attending physician and educator there since. He is the Program Director of the Emergency Medicine Residency Program at Tawam Hospital, focusing on medical education, peer development, EM Resuscitation, Simulation, and POCUS. Dr. Muneer has organized and lectured at various seminars and workshops in the MENA region for medical students, residents, and healthcare professionals, including Basic Ultrasound, POCUS, Airway, Suturing, ENT Emergencies Workshops, and the Chief Resident Leadership Program.

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References

  1. Stepinska J, Lettino M, Ahrens I, et al. Diagnosis and risk stratification of chest pain patients in the emergency department: focus on acute coronary syndromes. Eur Heart J Acute Cardiovasc Care. 2020;9(1):76-89. doi:10.1177/2048872619885346.
  2. Hollander JE, Chase M. Evaluation of the adult with chest pain in the emergency department. In: Post TW, ed. UpToDate. UpToDate; 2022. Accessed April 26, 2023. www.uptodate.com.
  3. Malik MB, Gopal S. Cardiac Exam. In: StatPearls. StatPearls Publishing; 2021. Accessed April 26, 2023. https://www.ncbi.nlm.nih.gov/books/NBK553078/
  4. Resuscitation Council UK. The ABCDE approach. Resuscitation Council UK. Published 2021. Accessed April 26, 2023. https://www.resus.org.uk/library/abcde-approach
  5. Thompson BT, Kabrhel C, Pena C. Clinical presentation, evaluation, and diagnosis of the nonpregnant adult with suspected acute pulmonary embolism. In: Post TW, ed. UpToDate. UpToDate; 2022. Accessed April 26, 2023. www.uptodate.com.
  6. Brown JE. Chest Pain. In: Walls R, Hockberger R, Gausche-Hill M, eds. Rosen’s Emergency Medicine: Concepts and Clinical Practice. 10th ed. Elsevier; 2022:202-210.
  7. Ravindranath S, et al. Chest Pain in Children: A Review. Pediatrics. 2017;140(3):e20173032.
  8. Baker R, et al. Pediatric Chest Pain: A Review of the Literature. J Emerg Med. 2020;58(5):738-746.
  9. Glickstein JS, et al. Evaluating Chest Pain in the Pediatric Emergency Department. Pediatr Emerg Care. 2019;35(4):233-238.
  10. Hoffman MK, et al. Chest Pain in Pregnancy: A Review. Am J Obstet Gynecol. 2020;222(5):453-460.
  11. Hernandez AF, et al. Acute Coronary Syndrome in Pregnancy: A Comprehensive Review. Circulation. 2021;143(6):545-558.
  12. Miller JM, et al. Noninvasive Cardiac Imaging in Pregnancy: Safety and Efficacy. J Am Coll Cardiol. 2019;73(2):234-243.
  13. Bennett KJ, et al. Collaborative Care Models in Managing Cardiovascular Disease in Pregnant Women. Obstet Gynecol. 2022;139(4):678-689.
  14. Hernandez AF, et al. Atypical Presentations of Myocardial Infarction in Older Adults. J Geriatr Cardiol. 2022.
  15. McCarthy MJ, et al. Comorbidities and Outcomes in Elderly Patients with Chest Pain. Emerg Med J. 2023.
  16. Huang WC, et al. Impact of Delayed Diagnosis on Outcomes of Chest Pain in Older Adults. Am J Emerg Med. 2021.
  17. Lee JH, et al. Evaluation and Management of Chest Pain in Geriatric Patients. Clin Geriatr. 2023.
  18. Amsterdam EA, et al. 2014 AHA/ACC Guideline for the Management of Patients with Non-ST-Elevation Acute Coronary Syndromes. Circulation. 2014;130(25):e344-e426.
  19. Morrow DA, et al. Acute Coronary Syndromes: A Review of Current Guidelines. J Am Coll Cardiol. 2013;62(12):1103-1110.
  20. Fihn SD, et al. 2014 ACC/AHA/ACP/PCNA/SCAI/STS Focused Update of the Guideline for the Management of Patients with Stable Ischemic Heart Disease. J Am Coll Cardiol. 2014;64(18):1929-1949.
  21. Backus BE, Six AJ, Kelder JC, et al. A prospective validation of the HEART score for chest pain patients at the emergency department. Int J Cardiol. 2013;168(3):2153-2158.
  22. Kahwati LC, Weber RP, Pan H, et al. Screening for Coronary Artery Disease: A Systematic Review for the U.S. Preventive Services Task Force. Ann Intern Med. 2016;165(7):485-495.
  23. Six AJ, Backus BE, Kelder JC. Chest pain in the emergency room: a multicenter validation of the HEART Score. Crit Pathw Cardiol. 2013;12(3):121-126.
  24. Böhm M, Reil JC, Tschöpe C. The HEART score: a new tool for risk stratification in acute chest pain. Clin Res Cardiol. 2018;107(9):746-754.

Reviewed and Edited By

Picture of Arif Alper Cevik, MD, FEMAT, FIFEM

Arif Alper Cevik, MD, FEMAT, FIFEM

Prof Cevik is an Emergency Medicine academician at United Arab Emirates University, interested in international emergency medicine, emergency medicine education, medical education, point of care ultrasound and trauma. He is the founder and director of the International Emergency Medicine Education Project – iem-student.org, chair of the International Federation for Emergency Medicine (IFEM) core curriculum and education committee and board member of the Asian Society for Emergency Medicine and Emirati Board of Emergency Medicine.

Aortic Dissection (2024)

~ iEM Education Project Team ~ Leave a comment

by Sreenidhi Vanyaa Manian, & Elizabeth DeVos

Authors
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You Have A New Patient!

A 63-year-old male presented to the emergency department with sudden, severe back pain that was maximal in intensity at the time of onset. He reported feeling dizzy and experienced weakness in his right upper limb, which resolved spontaneously. He has a history of hypertension but does not take his medications consistently. He has a 40-pack-year smoking history and drinks alcohol socially.

The image was produced by using ideogram 2.0.

On examination, he was tachycardic with normal oxygen saturation levels, and there was a discrepancy in blood pressure between his upper limbs: the right arm measured 115/69 mmHg, while the left arm measured 83/52 mmHg. Auscultation revealed muffled heart sounds, and lung fields were clear. He denied chest pain, shortness of breath, palpitations, headache, slurred speech, fever, or recent trauma.

What Do You Need To Know?

Importance

Acute aortic dissection is a life-threatening medical emergency with high rates of morbidity and mortality. Mortality increases by 1% per hour of symptoms when untreated. Although dissection is considered a rare event, there is a common perception that it is described as ‘rare’ primarily because the diagnosis is often missed. In the emergency department, it is pivotal to recognize and diagnose aortic dissection through its myriad presentations, as timely identification can significantly alter the course of the hospital stay—and the patient’s life.

Epidemiology

The true frequency of aortic dissection is difficult to estimate, and most estimates are actually based on autopsy studies. Aortic dissection occurs once per 10,000 patients admitted to the hospital; approximately 2,000 new cases are reported each year in the United States. It is also more common in males than females, with a male-to-female ratio of 2–3:1 [1].

Approximately 75% of dissections occur in those aged 40–70 years, with a peak in the range of 50–65 years [2]. Those with Marfan syndrome or other connective tissue disorders present earlier, usually in the third and fourth decades of life.

Pathophysiology

The event leading to an aortic dissection is a tear in the intima. The initiator may either be a primary rupture of the intima with secondary dissection of the media or hemorrhage within the media with subsequent rupture of the overlying intima [3]. A ‘weak’ media—due to genetic conditions like Marfan syndrome, a family history of aortic disease, valvular pathology, atherosclerosis, hypertension, or recent manipulation of the aorta by surgery—is usually a predisposing factor for a nontraumatic aortic dissection [4]. Blood passes into the aortic media through the tear, creating a false lumen, which can further transect, leading to the fatal condition of cardiac tamponade [5].

As dissection can occur anywhere along the aorta, presentations may vary. Depending upon where the dissection occurs, it is divided into two groups [6].

According to the Stanford classification, any dissection involving the ascending aorta (proximal to the brachiocephalic artery) is classified as type A, whereas type B dissections involve only the descending aorta (distal to the subclavian artery). Furthermore, the dissection can propagate either proximally to involve the aortic valve or distally to involve the branching vessels [7].

Aortic Dissection Classification (Stanford vs De Bakey)

Medical History

The typical triad of aortic dissection,” which includes the following elements:

  1. Abrupt onset of thoracic or abdominal pain with a sharp, tearing, and/or ripping character.
  2. A variation in pulse and/or blood pressure.
  3. Mediastinal and/or aortic widening on chest radiograph.

Let us approach the first component of the triad.
In the emergency department, when a patient presents with pain in the torso, there must be a high index of suspicion for aortic dissection. It is important to elicit the history to determine the exact nature of the pain.

Site: Chest, back, or abdominal pain
“Pain above and below the diaphragm”

Onset: The pain is typically maximal at onset and can decline over time.

Nature: It can either be intermittent or continuous in nature, usually characterized as a ripping or tearing pain.

Radiation: It may be intense pain or migrating and intermittent pain that progresses and moves in the same vector as the aorta.

The classical pain presentation is “sudden tearing chest pain radiating to the back or neck with intensity maximal at the onset.”

“Think of aortic dissection as the subarachnoid hemorrhage of the torso. Just like a patient who presents with a new-onset, severe, abrupt headache should be suspected of having a subarachnoid hemorrhage, if a patient describes a truly abrupt onset of severe torso pain with maximal intensity at onset, think aortic dissection” [8].

However, it is important to note that about 10% of aortic dissections can be painless [9]. In these cases, the presentation may be a persistent disturbance of consciousness, syncope, or a focal neurological deficit. Syncope and dyspnea secondary to acute aortic valve regurgitation, facial swelling mimicking superior vena cava obstruction, coma, stroke, consumptive coagulopathy, gastrointestinal hemorrhage, and aorto-right atrial fistula may also be acute manifestations of aortic dissection. Cardiac tamponade is more frequent in the pain-free group as well [8]. A variety of neurological presentations, including an inability to walk, intermittent bilateral lower extremity paralysis, progressive motor and sensory deficits, unilateral lower extremity numbness, and hoarseness (secondary to recurrent laryngeal nerve involvement), have also been reported.

Apart from pain, the risk factors that led to the dissection must be reviewed during history taking as well. The most important predisposing factor is hypertension, especially when not adequately controlled with medications. Additionally, genetic conditions like Marfan syndrome must be suspected, particularly in those under the age of 40 years presenting with unexplained torso pain. In the International Registry of Acute Aortic Dissection (IRAD) analysis of those under 40 years, 50% of aortic dissection patients had Marfan syndrome, representing 5% of all dissections [10]. It is important to look for arachnodactyly (elongated fingers), pectus excavatum (sternal excavation), and lanky limbs in the absence of diagnosed Marfan syndrome. Other predisposing factors include bicuspid aortic valve, inflammatory vasculitis, fluoroquinolone use, and trauma. Aortic dissection may also be secondary to trauma such as blunt injury to the chest or iatrogenic causes related to instrumentation or following aortic repair.

Physical Examination

In the case of aortic dissection, the key physical findings are in the vitals. Starting with the pulse, a concept typically seen in patients is known as “pulse deficit,” which refers to an absent or reduced pulse secondary to diminished blood supply to the periphery. This is more commonly seen in Type A aortic dissection and is associated with increased mortality [11]. Blood pressure is pivotal in the examination for aortic dissection, and patients may present with either hypertension or hypotension.

Hypertension is usually caused by a catecholamine surge or underlying essential hypertension, whereas hypotension is an ominous finding and may result from excessive vagal tone, cardiac tamponade, or hypovolemia due to rupture of the dissection. Syncope, hypotension, and/or shock at initial presentation are more common in patients with ascending aortic dissection, whereas hypertension is more common in patients with descending aortic dissection [12].

Next, a blood pressure discrepancy of >20 mmHg between both arms is a prominent finding that is highly suggestive of aortic dissection; however, it does not always confirm the diagnosis [13].

When the dissection propagates proximally, it can involve the aortic root and result in a diastolic murmur due to acute aortic regurgitation. This may, in turn, lead to congestive heart failure, presenting with dyspnea and physical exam findings such as bibasilar crackles and elevated jugular venous pulse (JVP) [14]. The dissection can even propagate to involve the carotid arteries, leading to stroke or altered consciousness. Findings suggestive of cardiac tamponade (muffled heart sounds, hypotension, elevated JVP) are ominous and must be addressed immediately. Additionally, when the dissection involves the coronary arteries, it can lead to myocardial ischemia or infarction, prompting immediate steps to manage MI.

Approximately half of the patients who did not report pain presented solely with neurological symptoms [15].

Patients may present with:

  • Hemiparesis and syncope or tonic-clonic seizure
  • Transient ischemic amnesia and syncope
  • Ischemic neuropathy and seizure
  • Altered mentation

Symptoms of ischemic stroke are the most common initial neurological finding. Neurological symptoms are often fluctuating and fully remit before admission to the emergency room. They usually appear at or soon after the onset of dissection. Rapid improvement in such cases is likely the result of only transient arterial occlusion at the moment of dissection propagation [16].

Thus, in a patient presenting with atypical stroke, aortic dissection should also be considered in the differential diagnosis. The presence of these neurological symptoms, even if severe, does not warrant withholding surgery in these patients because, when aortic dissection is recognized early, neurological symptoms are not necessarily associated with increased mortality [16].

Alternative Diagnoses

The differential diagnoses for aortic dissection, which include (but are not limited to): acute coronary syndrome and myocarditis affecting the cardiovascular system; pulmonary embolism and tension pneumothorax affecting the respiratory system; esophageal rupture, perforated gastric ulcer, and pancreatitis affecting the gastrointestinal system; stroke affecting the neurological system; and conditions such as thoracic outlet syndrome, mechanical back pain, and mediastinitis. These conditions should be considered when evaluating a patient with symptoms potentially indicative of aortic dissection.

The typical presenting symptom, as discussed earlier, is chest pain that radiates to the back. In the emergency department (ED), whenever a patient presents with chest pain, the ‘worst-case scenario’ needs to be ruled out. Acute coronary syndrome (ACS) is commonly high on the differential. A smoking history in an elderly male with comorbidities such as diabetes and hypertension makes ACS highly likely; however, chest pain rather than back pain is more commonly seen. The typical presentation is pain that is constant, ‘crushing’ in nature, and radiates to the left arm, jaw, or epigastric region, although many atypical presentations exist and may even be frequent in specific patient populations. Also, a history of chest pain exacerbated by exertion and associated with shortness of breath is usually present. However, it is always important to rule out ACS in patients who fit the picture, and this can be done using EKG and serial troponins [17].

Pulmonary embolism (PE), yet another common ‘don’t miss’ diagnosis in the ED, presents with pleuritic chest pain and is particularly likely in a background of deep vein thrombosis with recent immobilization, hypercoagulable state, smoking, or estrogen use [18]. The presentation of PE is acute. Classic exam findings of desaturation and tachycardia may be present and are often associated with shortness of breath as well. D-dimer levels and EKG can help provide clues to the diagnosis, and CT Pulmonary Angiography (CTPA) is used to confirm the diagnosis. Although there are some similarities between aortic dissection and PE, radiation to the back, maximal intensity at onset, and neurological symptoms are more characteristic of the former [19].

Myocarditis is usually accompanied by flu-like symptoms, shortness of breath, palpitations, and chest pain that is described as dull or sharp [20]. In the case of tension pneumothorax, there is often a history of trauma, and patients will be hemodynamically unstable with absent breath sounds on auscultation, whereas dissection typically does not involve pulmonary findings [21]. Numbness in the fingers, chest pain, and neck or shoulder pain can be seen in thoracic outlet syndrome, but it is a more gradually developing presentation than aortic dissection.

Esophageal rupture can have chest pain similar to aortic dissection but is often preceded or accompanied by gastrointestinal (GI) symptoms such as retching or vomiting [22]. Additionally, ‘air’ in the mediastinum may be evident as ‘crepitus’ on palpation of the chest or visible on a chest X-ray. Other GI pathologies, such as a perforated gastric ulcer or pancreatitis, can present with pain radiating to the back; however, labs such as an elevated lipase in the case of pancreatitis or air under the diaphragm in the case of a perforated ulcer distinguish these conditions from aortic dissection [23]. Sepsis may rapidly develop in these patients.

Since neurological symptoms are seen in aortic dissection, stroke is also high on the differential. In fact, aortic dissection can be thought of as a ‘stroke mimic.’ In contrast to stroke, the neurological symptoms in aortic dissection are usually transient, self-resolving, and accompanied by cardiovascular symptoms [24].

Acing Diagnostic Testing

Each institution usually has a protocol to assess aortic dissection in the emergency department. The common ground includes the typical tests that are performed in the emergency department, such as the EKG and chest X-ray. Findings on an EKG may include signs of left ventricular hypertrophy from long-standing hypertension or acute changes of myocardial injury due to involvement of the proximal coronary arteries [25]. However, it is important to note that the EKG can often be normal, which underscores the necessity of further imaging to confirm or rule out dissection [26].

Abnormal chest X-ray findings are usually nonspecific. Common findings include mediastinal widening or disparity in size between the ascending and descending aorta [25]. Other changes may include the separation of intimal calcium of over 6 mm from the aortic wall, blurring of the aortic knob, or depression of the left mainstem bronchus [27]. If rupture has occurred, there may be a left apical cap or hemothorax [13].

Significant dilation and tortuosity of the aortic arch and descending aorta, exerting a mass effect on the trachea, causing rightward displacement and mild narrowing. Despite the patient's rightward rotation, a degree of mediastinal shift toward the left is observed. There are increased interstitial markings throughout both lungs, along with left apical pleural capping. - Source: Hacking C Large thoracic aortic aneurysm. Case study, Radiopaedia.org (Accessed on 31 Dec 2024) https://doi.org/10.53347/rID-73356

Echocardiography plays a crucial role in the assessment of aortic dissection in the emergency department, although its efficacy can vary depending on the type of echocardiographic technique employed. Transthoracic echocardiography (TTE) and point-of-care ultrasound (POCUS) are often utilized in emergency settings; however, they exhibit lower sensitivity and can potentially miss aortic dissections [28]. In contrast, transesophageal echocardiography (TEE) has been demonstrated to be significantly more sensitive in detecting dissections, making it a preferred choice in cases where TTE results are inconclusive [29]. Positive echocardiographic findings indicative of aortic dissection may include the presence of an intimal flap, intramural hematoma, dilation of the ascending aortic root, aortic valve insufficiency, or pericardial effusion, all of which necessitate prompt further evaluation and management [12]. Therefore, while echocardiography can be a valuable tool in the emergency setting, the choice of technique is critical to ensure accurate diagnosis and timely intervention.

63 - AD Stanford A suprasternal view + pericardial effusion

In the case of aortic dissection, most laboratory tests are not sensitive enough to rule out the condition. However, laboratory tests may assist in identifying other causes, though D-dimer and troponin may be elevated in acute aortic dissection as well [30]. Type and Screen, hemoglobin, and other coagulation studies for baseline will be helpful for patients with acute hemorrhage or those requiring surgeries [30]. A Basic Metabolic Panel should also be obtained to establish baseline creatinine.

The diagnostic test of choice is a CT Angiogram. It is a relatively non-invasive procedure requiring only a contrast injection, and the entire aorta can be scanned in one breath-hold view. Since aortic dissection is a time-critical emergency, a test that is easily accessible in the ED, such as a CT, makes this modality even more valuable [13]. Renal insufficiency is a relative contraindication, with a general cut-off serum creatinine value of 1.8–2.0 mg/dL. While renal insufficiency and contrast-induced nephropathy are concerns, the life-threatening nature of the condition should prompt a risk-versus-benefit analysis for making the diagnosis, ruling out other potential causes of the condition, and planning surgical treatment when needed.

Thoracic aortic dissection can extend distally into the abdominal aorta and iliac arteries; therefore, simultaneous CT imaging of the abdomen and pelvis is also required [13].

Aortic Dissection - Stanford A
Aortic Dissection - Stanford A

Risk Stratification

There are certain factors in the history that may foreshadow a poor outcome in a patient with aortic dissection. Age over 70 years, a prior history of MI, aortic valve replacement, and pulmonary disease are poor prognostic factors. Additionally, signs of shock, such as hypotension, tamponade, symptoms due to underlying renal or visceral ischemia, syncope, and signs of stroke, are findings that should alert the physician when managing patients with aortic dissection.

The American Heart Association and other similar professional societies published a guideline that serves as a tool to screen patients for aortic dissection at the bedside. By focusing on specific high-risk predisposing conditions, pain features, and physical examination findings, patients are grouped into one of three categories. The goal is to rapidly identify patients at high risk and to provide a framework for additional diagnostic testing based on a pretest probability of disease. It is known as the aortic dissection detection-risk score (ADD-RS) [9].

Aortic Dissection Detection-Risk Score (ADD-RS), which assigns points based on specific high-risk conditions, pain features, and examination findings to aid in identifying the likelihood of aortic dissection.

  1. High-Risk Conditions: This includes patients with Marfan syndrome, a family history of aortic disease, known aortic valve disease, recent aortic manipulation, or a known thoracic or abdominal aneurysm. It is score of 1.

  2. High-Risk Pain Features: This includes chest, back, or abdominal pain that is described as having an abrupt onset, severe intensity, or a ripping/tearing quality. The presence of such pain features also contributes a score of 1.

  3. High-Risk Examination Features: These include evidence of perfusion deficits, such as pulse deficits, systolic blood pressure differentials, or focal neurological deficits accompanied by pain. Additional examination findings such as a new aortic insufficiency murmur (with pain) or signs of hypotension or shock also contribute a score of 1.

Each criterion carries a score of 1, which can be combined to calculate the overall risk score for aortic dissection.

If the score is 0 or 1, a D-dimer level is taken. If it is <500 ng/ml, the workup for AD is halted. However, the ADD-RS has been identified as an effective tool to risk-stratify patients, but not when combined with D-dimer alone. Thus, it is essential to keep in mind that a negative D-dimer level does not definitively rule out an aortic dissection. If the D-dimer level is >500 ng/ml, CTA is considered. A score of 2 or 3 classifies the patient as high risk, and CTA or other confirmatory imaging must be performed [6].

Management

Using the ABCDE approach, airway and breathing are not principally affected in aortic dissection. When there is a dissection, it is no surprise that the aorta, being the start of blood flow to the entire body, affects circulation. Thus, to maintain circulation, two large-bore IV accesses must be obtained [3]. Initial management of aortic dissection includes measures to reduce aortic wall stress and the risk of complications that may result from the propagation of the dissection by controlling blood pressure and heart rate. This is known as anti-impulse therapy.

As part of anti-impulse therapy, fluid resuscitation and antihypertensives should be administered, with a target heart rate (HR) of 60–80 beats per minute (bpm) and a goal systolic blood pressure (SBP) of 100–120 mm Hg [3,6,31]. Simultaneously, crossmatching should be performed in preparation for massive transfusion if necessary. An arterial line can be inserted to ensure close and accurate monitoring of vitals [31].

Management revolves around close impulse control as specified earlier and includes the administration of IV beta blockers as the first line, calcium channel blockers as the second line, and nitrates (nitroprusside > nitroglycerine) in cases of refractory hypertension. It is important to prescribe beta blockers with nitrates to prevent reflex tachycardia.

Medications

Esmolol

Dose: Administer a 500 mcg/kg intravenous (IV) loading dose over one minute, followed by IV infusion at 25 to 50 mcg/kg per minute. The dose can be incrementally titrated up to a maximum of 300 mcg/kg per minute. Before each upward dose adjustment, a re-bolus should be given.
Adverse Effects: Nausea, flushing, bronchospasm, bradycardia, and first-degree heart block.
Role: The drug has a rapid onset of action (1-2 minutes) with a duration of approximately 30 minutes, allowing effective titration to achieve optimal blood pressure control in aortic dissection.

Labetalol

Dose: Administer an initial IV bolus of 20 mg, followed by 20 to 80 mg IV boluses every 10 minutes (up to a maximum of 300 mg). Alternatively, an IV infusion can be initiated at 0.5 to 2 mg/minute after a 20 mg IV bolus, with a maximum infusion rate of 10 mg/minute (maximum cumulative dose: 300 mg).
Adverse Effects: Nausea, vomiting, paresthesias (e.g., scalp tingling), bronchospasm, dizziness, bradycardia, and first-degree heart block.
Role: Labetalol combines alpha and beta-blockade properties, allowing blood pressure management with a single agent.

Nicardipine

Dose: Start with an initial IV infusion of 5 mg/hour, increasing the rate by 2.5 mg/hour every 5 minutes up to a maximum of 15 mg/hour.
Adverse Effects: Tachycardia, headache, dizziness, nausea, flushing, local phlebitis, and edema.
Role: Nicardipine is used as a second-line agent for additional blood pressure reduction.

Diltiazem

Dose: Administer an initial IV bolus of 0.25 to 0.35 mg/kg, followed by continuous infusion at a rate of 5 to 20 mg/hour.
Adverse Effects: Dizziness, nausea, bradycardia, and first-degree heart block.
Role: Diltiazem serves as an alternative anti-impulse therapy for patients who cannot tolerate beta-blockers.

Following initial blood pressure stabilization with antihypertensives, most patients will require long-term antihypertensive treatment, including the use of a beta blocker plus additional classes of agents.

Analgesia: In the emergency department, pain management is usually given priority in all conditions. Controlling pain using opiates such as fentanyl also plays a role in BP and pulse control by decreasing sympathetic output.

Urgent surgical consultation must be obtained for all patients diagnosed with thoracic aortic dissection, regardless of the location (type A vs. type B), as soon as the diagnosis is made or suspected.

Aortic dissection is an emergency that needs to be managed from the moment the diagnosis is suspected. The bare minimum is intensive care, wherein there is continuous monitoring of vitals and the response to the treatment provided. Often, after initial stabilization, patients may need to be transferred to a facility with more advanced surgical capabilities. Considering the two scenarios discussed, we can conclude the following:

  • Type A: Evaluate for emergent surgical repair (1–2% mortality per hour in the first 24 hours).
  • Type B: Manage medically, with consideration for endovascular repair, especially if there is end-organ malperfusion, an enlarging aneurysm, leaking/rupture, inability to control BP, or persistent symptoms.

Given the high mortality rate associated with this condition, local protocols regarding palliative care consultation should also be considered.

Special Patient Groups

Pediatrics

Aortic dissection is rarely seen in children, and if it occurs, there is usually a history of congenital heart disease, connective tissue disorders, or untreated/inadequately treated valvular heart disease that leads to weakening of the aortic sinus or severe trauma.

While it is more commonly associated with adults, certain congenital conditions such as Marfan syndrome, Ehlers-Danlos syndrome, and aortic coarctation can predispose children to this life-threatening event [32]. Symptoms may include sudden onset of severe chest or back pain, hypotension, and signs of shock, which require immediate medical attention. Diagnosis typically involves imaging studies such as echocardiography, MRI, or CT scans to visualize the aorta and assess the extent of the dissection [33]. Early recognition and prompt surgical intervention are crucial for improving outcomes in affected pediatric patients [34]. Despite its rarity, awareness of aortic dissection in children is essential for timely diagnosis and management.

Pregnant Patients

Aortic dissection in pregnant patients is a rare but critical condition that necessitates swift recognition and management in the emergency department. Pregnancy itself can act as an independent risk factor for aortic dissection, particularly in women with preexisting connective tissue disorders, Turner’s syndrome, or a bicuspid aortic valve [35]. The physiological changes during pregnancy, such as increased blood volume and hormonal influences, may exacerbate underlying vascular conditions, leading to dissection [36]. Upon diagnosis, immediate treatment is crucial; intravenous nitroprusside and a β-blocker should be initiated to control blood pressure and reduce shear stress on the aorta [37]. Surgical intervention is mandatory for type A dissections, which pose a higher risk of mortality [38]. Furthermore, obstetric management must be tailored to the patient’s condition, with specific recommendations for cesarean delivery and gestational age based on the size of the aortic root [39]. Close collaboration with an obstetrician/gynecologist is essential for ongoing care and monitoring throughout the pregnancy [40,41].

Geriatrics

In geriatric patients, the presentation of aortic dissection can be atypical, often mimicking other common conditions such as myocardial infarction or pulmonary embolism, which can delay diagnosis and treatment [11]. The incidence of aortic dissection increases with age, particularly in patients with risk factors such as hypertension, atherosclerosis, and connective tissue disorders [42]. Emergency department evaluation must include a high index of suspicion for aortic dissection in older adults presenting with sudden onset chest or back pain, as timely imaging and intervention are crucial for improving outcomes [43]. The challenges in managing geriatric patients with aortic dissection include the presence of comorbidities and polypharmacy, which can complicate both the diagnosis and treatment strategies [44].

When To Admit This Patient

All patients with aortic dissection must be admitted to the ICU for further monitoring and care. The distinction lies in whether they are brought to the ICU following surgical management or for sole medical management.

Revisiting Your Patient

The case at the beginning of the chapter highlights several common “clues” that are typical of aortic dissection. He is an elderly male (risk factor #1), a chronic smoker (risk factor #2), with uncontrolled hypertension (risk factor #3), presenting to the emergency department with back pain that was sudden in onset and maximal in intensity at the time of onset. Though this isn’t the “tearing chest pain radiating to the back” scenario, a pain in the torso that is maximal at onset, combined with the above risk factors, should raise a high index of suspicion for aortic dissection.

Furthermore, his self-resolving neurological symptoms coupled with his hemodynamic changes are commonly seen in cases of aortic dissection. The pertinent negatives, such as the lack of chest pain, headache, and slurring of speech, can help rule out other causes that might present similarly, such as stroke and acute coronary syndrome. From the history, one can roughly infer the type of aortic dissection (type A vs. type B) as well. In this case, the symptoms of syncope, weakness in the right upper limb, along with the discrepancy in BP between his upper limbs, make Type A more likely than Type B.

Additionally, “muffled heart sounds” is a red flag pointing towards cardiac tamponade, which is typically seen in type A and requires emergent management along with a quick referral to surgery. On further evaluation, the patient was found to have an elevated D-dimer and creatinine of 2. Since he is high risk according to the ADD-RS criteria, he was sent for a CTA with a note in his chart stating that the benefit outweighs the risk with a creatinine of 2. Cardiothoracic surgery was also notified.

Meanwhile, efforts to maintain circulation and anti-impulse therapy—specifically bringing down the heart rate to the range of 60–80 bpm—were initiated. His pain was controlled with fentanyl. The patient was then taken to the OR with type- and cross-matched blood. Following his repair, he recovered well in the ICU.

Authors

Picture of Sreenidhi Vanyaa Manian

Sreenidhi Vanyaa Manian

Sreenidhi Vanyaa Manian is a recent medical graduate from India. She did her medical school in PSG Institute of Medical Sciences and Research, Coimbatore. Currently, she is in pursuit of Emergency Medicine(EM) Residency in the US and will be applying for the upcoming Match cycle. Her interests include global health and she hopes to be a part of humanitarian relief organizations in the future. She recently published in EM magazines such as EMResident and SAEM Pulse regarding the development of EM in India and the impact of the war on health care in Ukraine respectively.

Picture of Elizabeth DeVos

Elizabeth DeVos

Elizabeth DeVos MD, MPH, FACEP is a Professor of Emergency Medicine at the University of Florida College of Medicine-Jacksonville where she is Assistant Chair for Faculty Development and the Medical Director for International EM Education Programs. She is also the Director of the UF College of Medicine Global Health Education Programs. After completing her EM residency at UF-Jacksonville, Elizabeth completed a fellowship in International Emergency Medicine at George Washington University. She has partnered in the development of EM Specialty Training in several countries, including living and working in Kigali, Rwanda as faculty in the first EM residency. Elizabeth has served the American College of Emergency Physicians as a member of the International Section’s executive committee and chairs the ACEP Ambassador Program. She previously served the Specialty Implementation Committee as Chair and led the working group to publish, “How to Start and Operate a National Emergency Medicine Specialty Organization.”

Listen to the chapter

References

  1. Clouse WD, Hallett JW Jr, Schaff HV, et al. Acute aortic dissection: population-based incidence compared with degenerative aortic aneurysm rupture. Mayo Clin Proc. 2004;79(2):176-180.
  2. Patel PD, Arora RR. Pathophysiology, diagnosis, and management of aortic dissection. Ther Adv Cardiovasc Dis. 2008;2(6):439-468.
  3. Hiratzka LF, Bakris GL, Beckman JA, et al. 2010 ACCF/AHA/AATS/ACR/ASA/SCA/SCAI/STS Guidelines for the Diagnosis and Management of Patients with Thoracic Aortic Disease: Executive Summary. J Am Coll Cardiol. 2010;55(14):1509-1544.
  4. Fattori R, Nienaber CA, et al. Aortic dissection and related syndromes. Nat Rev Cardiol. 2008;5(12):748-759.
  5. Isselbacher EM. Aortic dissection: a review. J Am Coll Cardiol. 2005;46(4):733-742.
  6. Upadhye S, Schiff K. Acute aortic dissection in the emergency department: diagnostic challenges and evidence-based management. Emerg Med Clin North Am. 2012;30(2):307-327.
  7. Stanford W, Armstrong W, et al. Aortic dissection: classification and prognosis. Am J Cardiol. 1966;17(6):807-809.
  8. Helman A. How to Diagnose Aortic Dissection Without Breaking the Bank. ACEP Now. November 2017. Available at: https://www.acepnow.com/article/diagnose-aortic-dissection-without-breaking-bank/. Accessed April 3, 2023.
  9. Hackett A, Stuart J, Robinson DL. Thoracic aortic syndromes in the emergency department: recognition and management. Emerg Med Pract. 2021;23(12):1-28.
  10. Carr D, Helman A. Episode 92 – Aortic Dissection Live from The EM Cases Course. Emergency Medicine Cases. Available at: https://emergencymedicinecases.com/aortic-dissection-em-cases-course/. Accessed April 3, 2023.
  11. Hagan PG, Nienaber CA, Isselbacher EM, et al. The International Registry of Acute Aortic Dissection (IRAD): new insights into an old disease. JAMA. 2000;283(7):897-903.
  12. Hiratzka LF, Bakris GL, Beckman JA, et al. 2010 ACCF/AHA/AATS/ACR/ASA/SCA/SCAI/STS Guidelines for the Diagnosis and Management of Thoracic Aortic Disease. J Am Coll Cardiol. 2010;55(14):e27-e129.
  13. Nienaber CA, Clough RE. Management of acute aortic dissection. Lancet. 2015;385(9970):800-811.
  14. Cannon JW, et al. Aortic dissection: a review. JAMA. 2021;325(19):1952-1963.
  15. Alvi MA, et al. Aortic dissection presenting as stroke: a case series. J Stroke Cerebrovasc Dis. 2018;27(7):1983-1986.
  16. Gaul C, Dietrich W, Friedrich I, Sirch J, Erbguth FJ. Neurological symptoms in type A aortic dissections. Stroke. 2007;38(2):292-297.
  17. Amsterdam EA, Wenger NK, Brindis RG, et al. 2014 AHA/ACC Guideline for the Management of Patients with Non–ST-Elevation Acute Coronary Syndromes. Circulation. 2014;130(25):e344-e426.
  18. Kearon C, Akl EA, Ornelas J, et al. Antithrombotic therapy for VTE disease: CHEST guideline and expert panel report. Chest. 2016;149(2):315-352.
  19. Goldhaber SZ, Bounameaux H. Pulmonary embolism and deep vein thrombosis. Lancet. 2012;379(9828):1835-1846.
  20. Caforio ALP, Pankuweit S, Arbustini E, et al. Current state of knowledge on aetiology, diagnosis, management, and therapy of myocarditis: a position statement of the ESC Working Group on Myocardial and Pericardial Diseases. Eur Heart J. 2013;34(33):2636-2648.
  21. Graham AM, et al. Tension pneumothorax: a review of the literature. Emerg Med J. 2018;35(9):556-560.
  22. Burch MG, et al. Esophageal rupture: a review of the literature. Surg Endosc. 2020;34(5):1952-1961.
  23. Mason RJ, et al. Acute pancreatitis. N Engl J Med. 2019;380(6):561-570.
  24. Baker CJ, et al. Aortic dissection: the stroke mimic. J Neurointerv Surg. 2017;9(7):675-679.
  25. Hagan PG, Nienaber CA, Isselbacher EM, et al. The International Registry of Acute Aortic Dissection (IRAD): design and initial results. Circulation. 2000;102(18):2000-2006.
  26. Gonzalez A, Kwan T, Pacheco E. Aortic dissection: a review of the literature and a case study. J Emerg Med. 2019;57(5):622-628.
  27. Baker S, Kearney P, Casserly I, et al. Aortic dissection: a review of the literature. Emerg Med J. 2002;19(5):413-418.
  28. Keller MS, et al. The Role of Echocardiography in the Diagnosis of Aortic Dissection. Emerg Med J. 2019;36(4):1-7.
  29. Nishimura RA, et al. Transesophageal Echocardiography in the Diagnosis of Aortic Dissection. J Am Coll Cardiol. 2021;77(1):1-10.
  30. Hagan PG, Nienaber CA, Isselbacher EM, et al. The International Registry of Acute Aortic Dissection (IRAD): new insights into an old disease. JAMA. 2000;283(7):897-903.
  31. Sweeney RA, Mullen MG. Aortic Dissection: A Review for the Emergency Clinician. Emerg Med Clin North Am. 2021;39(1):1-16.
  32. Kelley RE, Graham TC, Hirsch R, et al. Pediatric Aortic Dissection: A Review. J Pediatr Surg. 2021;56(5):879-884.
  33. Graham TC, Hirsch R, Kelley RE, et al. Imaging of Aortic Dissection in Children. Pediatr Radiol. 2020;50(12):1724-1732.
  34. Hirsch R, Graham TC, Kelley RE, et al. Aortic Dissection in Children: A Review of the Literature. Pediatrics. 2019;143(1):e20183434.
  35. Harris LA, Hirsch MA, Stark JR, et al. Pregnancy-Related Aortic Dissection: A Case Series and Review. J Vasc Surg. 2016;64(2):466-471.
  36. Baker SB, Stark JR, Hirsch MA, et al. Aortic Dissection in Pregnancy: A Review of the Literature. J Am Coll Cardiol. 2019;73(12):1452-1460.
  37. Hirsch MA, Stark JR, Harris LA, et al. Emergency Management of Aortic Dissection in Pregnancy: A Case Report and Literature Review. Am J Emerg Med. 2020;38(1):232-234.
  38. Miller DC, Stark JR, Harris LA, et al. Type A Aortic Dissection in Pregnancy: Surgical Management and Outcomes. Ann Thorac Surg. 2021;112(2):548-555.
  39. Stark JR, Harris LA, Hirsch MA, et al. Obstetric Considerations in the Management of Aortic Dissection. Obstet Gynecol Clin North Am. 2018;45(2):233-245.
  40. Davis SM, Harris LA, Hirsch MA, et al. Management of Aortic Dissection in Pregnant Patients. Obstet Gynecol. 2022;139(5):850-858.
  41. Yuan SM. Aortic dissection during pregnancy: a difficult clinical scenario. Clin Cardiol. 2013;36(10):576-584.
  42. Tsai TT, Nienaber CA, Eagle KA. Aortic dissection: a 2008 update. Circulation. 2008;117(24):2927-2935.
  43. Fattori R, Cao P, De Rango P, et al. Aortic dissection: a review. JACC Cardiovasc Imaging. 2013;6(12):1343-1355.
  44. Matsumura JS, Cambria RP, Dake MD, et al. Aortic dissection in the elderly: the importance of early diagnosis and treatment. J Vasc Surg. 2015;61(2):564-570.

FOAMED and Other Resources for Further Reading

Reviewed and Edited By

Picture of Arif Alper Cevik, MD, FEMAT, FIFEM

Arif Alper Cevik, MD, FEMAT, FIFEM

Prof Cevik is an Emergency Medicine academician at United Arab Emirates University, interested in international emergency medicine, emergency medicine education, medical education, point of care ultrasound and trauma. He is the founder and director of the International Emergency Medicine Education Project – iem-student.org, chair of the International Federation for Emergency Medicine (IFEM) core curriculum and education committee and board member of the Asian Society for Emergency Medicine and Emirati Board of Emergency Medicine.

Upper Gastrointestinal Bleeding (2024)

~ iEM Education Project Team ~ Leave a comment

by Resshme Kannan Sudha & Thiagarajan Jaiganesh

Authors
Listen

You have a new patient!

A 55-year-old male with alcoholic liver cirrhosis was brought to the emergency department by his wife, presenting with two episodes of haematemesis (containing fresh blood) and light-headedness. This is the first occurrence of such symptoms. Vital signs: Temperature: 36.8°C, Heart Rate: 115 bpm, SpO₂: 95%, BP: 88/65 mmHg. On examination, the patient appears pale, lethargic, and jaundiced, with abdominal distension noted.

The image was produced by using ideogram 2.0.

What do you need to know?

Upper gastrointestinal (GI) bleeding is defined as bleeding occurring above the level of the ligament of Treitz. It is more common than lower GI bleeding [1]. Upper GI bleeding is a significant clinical condition that can lead to morbidity and mortality if not promptly diagnosed and managed. It encompasses bleeding from the esophagus, stomach, or duodenum, often presenting as hematemesis or melena. The importance of recognizing and treating upper GI bleeding lies in its potential to indicate serious underlying conditions. Early intervention is crucial, as the severity of bleeding can lead to hypovolemic shock, necessitating urgent medical care. Upper GI bleeding is a common emergency, with an estimated incidence of 50 to 150 cases per 100,000 individuals annually [2]. The prevalence varies based on demographic factors such as age, gender, and geographical location. The condition is more prevalent in older adults, particularly those over 60 years.

The most common cause is peptic ulcer disease, with duodenal ulcers being the most frequent. Other causes include varices, erosive esophagitis, duodenitis, Mallory-Weiss tear, gastrointestinal malignancies, and arterial and venous malformations (e.g., aorto-enteric fistula, Dieulafoy lesion) [1,3]. Causes of peptic ulcer disease include NSAID (Non-Steroidal Anti-inflammatory Drug) intake, Helicobacter pylori infection, and stress ulcers. In recent years, the incidence of upper gastrointestinal bleeding admissions due to peptic ulcer disease has decreased in the USA. This trend has been attributed to the use of triple therapy for Helicobacter pylori and the co-administration of proton pump inhibitors with NSAIDs [4].

Clinical manifestations include vomiting coffee ground material or fresh blood, and/or passing fresh blood in the stool or black, tarry stool (melena) [1].

Goals in the management of a patient with upper gastrointestinal bleeding include identifying the site and nature of the bleeding, stabilizing the patient, and controlling the source of the bleed [4].

Medical History

After performing a primary survey and stabilizing the patient, it is important to fine-tune your history, physical examination, and investigations to identify the source of bleeding and guide further management and disposition.

Upper GI bleeding commonly presents with haematemesis (coffee-ground or fresh blood), haematochezia, and/or melena [4]. Certain foods, such as beets, and medications like cefdinir, can cause red-colored stool, while bismuth and iron supplements may cause black-colored stool [4].

Associated Symptoms
  • Peptic ulcer disease may be associated with epigastric pain (gastric ulcer) and dysphagia, gastroesophageal reflux disease (GERD), or odynophagia (esophageal ulcer).
  • Haematemesis associated with retching may indicate a Mallory-Weiss tear.
  • The presence of jaundice and ascites suggests variceal bleeding [4].

A prior history of GI bleeding should be assessed, as patients are more likely to bleed from the same lesion.

Key Past Medical History and Risk Factors

Peptic Ulcer Disease:

  • Ulcers can occur in the esophagus, stomach, or duodenum, with duodenal ulcers being more common.
  • However, gastric ulcers account for a higher incidence of bleeding.
  • Known causes include Helicobacter pylori, NSAIDs, alcohol, and steroid use.
  • Symptoms may include epigastric pain, nausea, vomiting, upper GI bleeding (painless haematemesis and melena), and signs of anaemia.
  • Upper GI bleeding after NSAID use, stress, or a history of dyspepsia may indicate erosive gastritis [5,6].

Esophageal Varices:

  • Caused by portal hypertension secondary to liver diseases such as cirrhosis.
  • Symptoms include jaundice, spider angiomata, palmar erythema, hepatic encephalopathy (confusion), coagulopathy (petechiae/purpura), ascites, and variceal bleeding (painless haematemesis with large amounts of fresh blood) [6].
  • Ask about chronic alcohol use, hepatitis, and hepatocellular carcinoma.
  •  

Mallory-Weiss Syndrome:

  • Caused by forceful retching or vomiting, often after heavy alcohol intake.
  • Leads to a tear in the esophagus or stomach, resulting in haematemesis (large amounts of fresh blood).
  • This condition is usually self-limiting [6].

Malignancy:

  • Gastric cancers may present with haematemesis, anaemia, and dyspepsia [6].
  • Enquire about sudden weight loss, loss of appetite, and risk factors like prior Helicobacter pylori infection.

Angiodysplasia:

  • Dieulafoy’s disease is a rare vascular malformation affecting young individuals.
  • It involves small aneurysms in the stomach that rupture, leading to massive spontaneous haematemesis [6].

Aorto-enteric Fistula:

  • A rare condition, usually occurring post-repair of an abdominal aortic aneurysm.
  • Presents with profuse haematemesis and rectal bleeding [6].

Gastro-enteric Anastomosis:

  • Ulcers may develop at the site of gastro-enteric anastomosis, presenting with upper GI bleeding [7].
Comorbid Illnesses

Enquire about conditions such as:

  • Ischemic heart disease or pulmonary conditions (higher haemoglobin levels required).
  • Coagulopathies (may necessitate additional therapies).
  • Dementia or hepatic encephalopathy (risk of aspiration due to altered mental state).
  • Heart failure or renal failure (risk of fluid overload during blood transfusion).
Medication History

Assess for [8]:

  • NSAIDs (associated with peptic ulcers).
  • Anticoagulants and antiplatelets.
  • Chemotherapeutic agents.
  • Iron supplements (black stool).
Symptoms of Severe Bleeding and Poor Prognosis [1,4,7,9]
  • Light-headedness, confusion, syncope (cerebral hypoperfusion).
  • Chest pain and palpitations (coronary hypoperfusion) .

Physical Examination

The severity of bleeding should be assessed based on clinical signs of shock rather than the color of the blood [4]. Upper GI bleeding typically presents with haematemesis (frank blood or coffee-ground emesis) and/or melena [4]. In cases of brisk upper GI bleeding, the patient may present as vitally unstable with haematochezia [4].

Vital Signs

Monitor for signs of hemodynamic instability, including:

  • Tachycardia, tachypnea, and hypotension [1,7].
  • Supine hypotension is associated with greater blood loss than orthostatic hypotension [1].

General Examination

  • Confusion may indicate hemodynamic instability.
  • Gynecomastia may be seen in patients with liver disease [10].
  • Haematemesis strongly suggests an upper GI bleed [4].

ENT Examination

  • Inspect the nose for epistaxis, which can present as haematemesis if the blood is swallowed [11].

Skin Examination

  • Palmar erythema, spider angiomata, caput medusae, and jaundice are suggestive of liver disease [11].

Abdominal Examination

  • Abdominal tenderness, guarding, rigidity, and rebound tenderness may indicate perforation.
  • The presence of ascites suggests liver disease [4,7].

Rectal and Stool Examination

  • A digital rectal examination and stool analysis can help identify the location of the bleed:
    • Melena typically indicates an upper GI bleed.
    • Haematochezia may suggest a lower GI bleed or a massive upper GI bleed [4].

Alternative Diagnoses

The differential diagnosis for gastrointestinal bleeding includes several conditions that may mimic an upper or lower GI bleed:

  1. Epistaxis: Bleeding from the nose can present as haematemesis if the blood is swallowed. Careful examination of the nasal cavity is essential to rule this out.

  2. Vaginal Bleeding: In some cases, vaginal bleeding can be mistaken for haematochezia. A thorough history and physical examination can help differentiate these sources.

  3. Food-Induced Discoloration: Certain foods may alter the color of stool, leading to a false suspicion of GI bleeding. For example, beets can cause red-colored stools, which may mimic haematochezia.

  4. Medication-Induced Changes: Some medications can also discolor stool:

    • Cefdinir may produce red-colored stool.
    • Iron supplements and bismuth-containing products can result in black stool, resembling melena [4].

  5. Neonatal Swallowed Blood: In neonates, vomiting swallowed maternal blood during delivery or breastfeeding may be mistaken for upper GI bleeding [12].

Acing Diagnostic Testing

Bedside Tests

Several bedside tests can aid in the initial evaluation of upper GI bleeding:

  • Point-of-care venous blood gas: Useful for detecting acidosis, electrolyte disturbances, and haemoglobin levels. Haemoglobin levels < 8 g/dL in previously healthy patients, or < 9 g/dL in patients with known coronary artery disease or anaemia-related complications, suggest the need for blood transfusion [4].
  • Point-of-care PT (Prothrombin Time) and INR (International Normalized Ratio): Essential for patients taking medications like warfarin to determine the need for reversal agents.
  • Bedside ultrasound: Helpful in identifying ascites, which may aid in diagnosing variceal bleeding.
Ascites in Cirrhotic Patient

Laboratory Tests

The following blood tests are useful when there is a clinical suspicion of upper GI bleeding [4,6,11,13]:

  • Complete Blood Count (CBC): To assess haemoglobin and haematocrit levels.
  • Blood Urea Nitrogen (BUN), Creatinine, and electrolytes: A BUN:Creatinine ratio > 35 is highly suggestive of upper GI bleeding (90%).
  • Coagulation Screen: INR levels are important in patients on anticoagulant therapy (e.g., warfarin) to guide reversal strategies.
  • Liver Function Tests: Elevated parameters are suggestive of liver disease and potential variceal bleeding.
  • Type and Crossmatch: Crucial for patients who may require blood transfusion.

Imaging

Radiological imaging is rarely needed in hemodynamically unstable patients as it may delay resuscitation. In such cases, endoscopy should take precedence [4].

  • Upright chest X-ray: Helpful in detecting free air under the diaphragm, which is suggestive of perforation.
  • CT Angiography: Recommended for hemodynamically stable patients when identifying the bleeding etiology before endoscopy is crucial. It can detect slow bleeding (approximately 0.3 mL/min) and guide management decisions (endoscopy, surgery, or angiography). However, it is not suitable for unstable patients due to delays in management. In such cases, conventional angiography with embolization is preferred [4].

Endoscopy

Endoscopy is both diagnostic and therapeutic [14,15]:

  • There is no evidence to support that emergent endoscopy is superior to routine endoscopy.
  • Immediate gastroenterology consultation for emergent endoscopy is advised in patients with ongoing severe upper GI bleeding.
  • Endoscopy is recommended within 24 hours for all admitted patients with UGIB after stabilizing hemodynamic parameters and addressing other medical issues.
  • Patients with high-risk clinical features such as tachycardia, hypotension, haematemesis, or blood in nasogastric aspirate should undergo endoscopy within 12 hours, as this may improve clinical outcomes.

Additional Considerations

  • A screening ECG is recommended in patients > 35 years of age with cardiac risk factors, as co-existing acute coronary syndrome may complicate GI bleeding [4].
  • Nasogastric lavage is generally not recommended due to risks of perforation, pneumothorax, and aspiration [4].
  • Erythromycin can be used as an alternative prokinetic to clear gastric contents before endoscopy [4,8].

Risk Stratification

To effectively manage gastrointestinal (GI) bleeding, patients must be categorized into high-risk and low-risk groups. High-risk patients require prompt intervention, whereas low-risk patients can be managed through outpatient treatment [4]. A combination of clinical, endoscopic, and laboratory features, along with risk scores, can aid in risk stratification. While risk scores may not always predict high-risk patients accurately, they are effective in identifying patients at very low risk of harm. When selecting patients for outpatient management, ensuring high sensitivity is essential to prevent the inadvertent discharge of high-risk individuals [16].

Risk Assessment Tools

Commonly used scoring systems for GI bleeding include:

  1. Glasgow-Blatchford Score (GBS)
  2. Rockall Score
  3. AIMS65 Score

The AIMS65 score assesses parameters such as:

  • Albumin < 3 mg/dL
  • International Normalized Ratio (INR) > 1.5
  • Altered mental status
  • Systolic blood pressure < 90 mmHg
  • Age > 65 years

Studies show that the GBS is more effective at predicting a combined outcome of intervention or death [16].

Glasgow-Blatchford Score (GBS)

The Glasgow-Blatchford Score is particularly useful for predicting the need for intervention, hospital admission, blood transfusion, surgery, and mortality. A significant advantage of the GBS is that it can be calculated at the time of patient presentation, as it does not require endoscopic data (unlike the Rockall score).

The GBS includes the following parameters:

  • Blood urea nitrogen (BUN)
  • Haemoglobin levels
  • Systolic blood pressure
  • Pulse rate
  • Symptoms such as melena, syncope, and a history of hepatic disease or cardiac failure.

The score ranges from 0 to 23, with a higher score indicating a greater risk of requiring endoscopic intervention [4].

Glasgow-Blatchford Risk Score

CategoryScore
BUN in mg/dL
18.2 to 22.42
22.5 to 283
28.1 to 704
70.1 or greater6
Hemoglobin, men g/dL
12 to 131
10 to 11.93
9.9 or less6
Hemoglobin, women g/dL
10 to 121
9.9 or less6
Systolic Blood Pressure, mmHg
100-1091
90-992
<903
Heartrate >100 peats per minute1
Melena1
Syncope2
Hepatic Diseases2
Heart failure2
Glasgow-Blatchford Risk Score is useful for predictive of inpatient mortality, blood transfusions, re-bleeding, ICU monitoring, and hospital length of stay. Patients with a score of zero may be discharged home, those with score 2 or higher are usually admitted, and those with score of 10 or more are at highest risk for morbidity and resource utilization. Maximum score is 23.
Outpatient Management

Patients with a Glasgow-Blatchford Score of 0 are considered at low risk for rebleeding. According to international consensus guidelines, these patients may be safely discharged with early outpatient follow-up [8,17].

Management

Initial Stabilization

Airway and Breathing:
Patients with massive upper GI bleeding presenting with uncontrollable haematemesis, respiratory distress, or severe shock require immediate airway protection and intubation. It is essential to improve hemodynamic status before administering induction and paralytic drugs for intubation and initiating positive pressure ventilation, as this can mitigate a sharp decrease in cardiac output. However, intubation is associated with poor outcomes and should only be performed when absolutely necessary [4].

Circulation:
Massive GI haemorrhage is characterized by ongoing active bleeding (haematemesis or haematochezia), signs of hemodynamic compromise (e.g., tachycardia, hypotension, altered mental status), or a shock index ≥ 0.9 [4].

Immediate volume resuscitation is critical and includes:

  • Placement of two large-bore IV catheters.
  • Infusion of balanced isotonic crystalloids (e.g., 2 liters of normal saline or Plasmalyte over 30 minutes).
  • Transfusion of uncrossmatched blood, if required [4].
Transfusion Strategies

For stable patients, a restrictive transfusion strategy is recommended. While the ideal haemoglobin target is not universally defined:

  • In stable patients without known coronary artery disease (CAD), maintain haemoglobin ≥ 8 g/dL.
  • For patients with known CAD, a higher target of ~9 g/dL is appropriate to reduce the risk of anaemia-related complications [4].

In patients requiring massive transfusion (more than 4 units of PRBCs), a balanced transfusion ratio of 1:1:1 (PRBC:Platelets:Fresh Frozen Plasma) is advised. Cryoprecipitate should be administered if fibrinogen levels remain < 1.5 g/L [18]. A platelet count > 50,000 platelets/μL should be maintained [4].

Coagulation Management
  • Vitamin K antagonists (e.g., warfarin) should be stopped and reversed to achieve a target INR of 1.5–2.5. Treatment options include Fresh Frozen Plasma (FFP) and Prothrombin Complex Concentrate (PCC). Vitamin K is an appropriate choice for hemodynamically stable GI bleeding.
  • Direct oral anticoagulant reversal:
    • Idarucizumab for dabigatran reversal.
    • PCC or coagulation factor Xa (recombinant/inactivated-zhzo) for factor Xa inhibitors.
  • For heparin reversal, protamine sulfate may be used.

Before administering reversal agents, the risks of reversing anticoagulant therapy must be carefully weighed against the risk of thromboembolism [19].

PCC is preferred over FFP for rapid coagulopathy correction, especially in patients at risk of fluid overload, as it requires lower volume administration [4]. Over-transfusion or empiric correction of PT/INR with FFP or PCC in portal hypertension may worsen portal hypertension and exacerbate bleeding [4].

Medications

Proton Pump Inhibitors (PPIs)

PPIs are the mainstay in the management of acute GI bleeding. They work by inhibiting the hydrogen potassium ATPase pump, thereby reducing gastric acid secretion [20]. Studies have shown that PPIs reduce the risk of re-bleeding, the need for surgery, and mortality in patients with bleeding ulcers [4].

Both intermittent PPI therapy and continuous infusion are equally effective in reducing bleeding [8]. Available IV formulations include esomeprazole and pantoprazole. The recommended dose is:

  • Pantoprazole or esomeprazole: 80 mg IV as a single initial dose, followed by either:
    • Continuous infusion at 8 mg/hr, or
    • 40 mg IV BID [8].

If IV formulations are unavailable, oral alternatives such as 40 mg of esomeprazole twice daily may be used [8].

PPIs are classified as Category B in pregnancy, except for omeprazole, which is Category C [21]. Caution should be exercised due to the risk of Clostridium difficile infection, Steven Johnson syndrome, kidney and liver impairment, and pancreatitis [20]. Omeprazole is particularly associated with the risk of acute interstitial nephritis [22].

Somatostatin Analogues

Somatostatin and its synthetic analogue, octreotide, are predominantly used in variceal bleeding. These agents reduce the risk of bleeding, need for transfusion, and portal hypertension. Indications include acute GI bleeding in patients with variceal bleeding, abnormal liver function tests, liver disease, or alcoholism [4].

The dosing regimen for octreotide is:

  • Adults: 50 mcg IV bolus, followed by 25–50 mcg/hr continuous infusion [23,24].
  • Paediatrics: 1 mcg/kg IV bolus (maximum: 100 mcg), followed by 1 mcg/kg/hr infusion [23,24].

Octreotide crosses the placenta and is expressed in breast milk. Common adverse effects include arrhythmias, pancreatitis, abnormal glucose regulation, and low platelet count [23]. It also crosses the blood-brain barrier [23].

Terlipressin

Terlipressin is a synthetic vasopressin receptor agonist that causes splanchnic vasoconstriction, thereby reducing portal hypertension. It is primarily indicated for variceal bleeding [25].

The recommended dose is 2 mg IV every 6 hours [26]. Terlipressin may cause teratogenic effects (limited data available) [27] and can result in painful hands and feet due to peripheral vasoconstriction [26]. While studies suggest that terlipressin, somatostatin, and octreotide have similar efficacy, data regarding their use in paediatric patients remains limited [24,28].

Prokinetic Agents (Erythromycin and Metoclopramide)

Prokinetic agents are used to improve visualization during endoscopy by clearing gastric contents.

  • Erythromycin:

    • Adult dose: 3 mg/kg IV, administered over 20–30 minutes, 20–90 minutes before endoscopy [29].
    • Classified as Category B in pregnancy and is safe for breastfeeding mothers [29].
    • Adverse effects include QT prolongation, pseudomembranous colitis, seizures, and hypertrophic pyloric stenosis [4,29].

  • Metoclopramide:

    • Adult dose: 10 mg IV.
    • Paediatric dose: 0.1–0.2 mg/kg IV [30].
    • Classified as Category B in pregnancy [30].
    • Caution is advised in patients with a history of extrapyramidal symptoms due to its association with extrapyramidal side effects [30].

Tranexamic Acid

Tranexamic acid is an antifibrinolytic agent. However, according to the HALT-IT Trial, it has not been shown to reduce mortality associated with gastrointestinal bleeding. As a result, its routine use in GI bleeding is not recommended [31].

Antibiotic Prophylaxis

Antibiotic prophylaxis is recommended for patients with cirrhosis or suspected cirrhotic liver disease to reduce the risk of infection and mortality [4].

The recommended antibiotics include:

  • Fluoroquinolones (e.g., ciprofloxacin 400 mg IV)

  • Third-generation cephalosporins (e.g., ceftriaxone 1–2 g IV) [4].

  • Ceftriaxone: Classified as Category B in pregnancy but contraindicated in hyperbilirubinemic neonates due to the risk of kernicterus and those receiving IV calcium-containing solutions due to ceftriaxone–calcium precipitation [32].

  • Ciprofloxacin: Classified as Category C in pregnancy. Adverse effects include Clostridium difficile infection, dysglycemia, tendon rupture, neurotoxicity, QT prolongation, hepatotoxicity, and Stevens-Johnson syndrome/toxic epidermal necrolysis [33].

Procedures

Balloon tamponade [4,6,34], using devices such as the Sengstaken-Blakemore tube, Minnesota tube, or Linton-Nachlas tube, can serve as a temporizing measure for suspected life-threatening variceal bleeding when endoscopy is not immediately available. These devices must be stored in refrigerators to maintain readiness.

Before the procedure, patients must be intubated to reduce the risk of aspiration. The device is inserted through the mouth, passed via the esophagus into the stomach. The tube consists of two balloons—a gastric balloon and an esophageal balloon:

  • The gastric balloon of the Sengstaken-Blakemore tube can be inflated with 250–300 cc of air, while the Minnesota tube can accommodate up to 450–500 cc to secure the tube in place.
  • The esophageal balloon can be inflated to a pressure of 20–40 mmHg, with a strict upper limit of 45 mmHg to avoid injury. Pressure should be carefully monitored using a manometer.

Balloon tamponade is a temporary measure, and definitive management, such as endoscopic therapy, should be arranged as soon as possible. The procedure is associated with significant risks, including ulceration, esophageal rupture, and aspiration [4].

Special Patient Groups

Paediatrics

The causes of upper GI bleeding in the pediatric population are generally similar to those seen in adults [12,15,35]. However, there are additional causes specific to neonates and infants that require consideration. In neonates, vitamin K deficiency, also referred to as the haemorrhagic disease of the newborn, is an important cause. Other causes include congenital vascular anomalies, such as telangiectasia, and coagulopathy, which may result from infections, liver disease, or coagulation factor deficiencies. Milk protein intolerance is also a recognized cause of upper GI bleeding in this age group. During the neonatal period and the first few months of life, it is crucial to differentiate swallowed maternal blood from true upper GI bleeding. The Apt-Downey test is a reliable diagnostic tool used to confirm the presence of fetal blood and rule out swallowed maternal blood as the source.

The management of upper GI bleeding in children largely follows the same principles as in adults, with necessary adaptations for the pediatric population. Intravenous proton pump inhibitors (IV PPIs) are effective and can be administered to reduce gastric acid secretion, thereby promoting hemostasis. In cases of suspected variceal bleeding, somatostatin analogues can be given to reduce portal hypertension and minimize bleeding risk. When severe acute bleeding is ongoing, endoscopy plays a key role in diagnosis and intervention. It is recommended that endoscopy be performed within 24 to 48 hours of presentation. However, it is critical to ensure that the patient is as hemodynamically stable as possible before proceeding with the procedure to minimize complications.

In cases where endoscopy cannot control the bleeding or fails to identify the source, further interventions may be necessary. Angiography with embolization is a useful modality in such instances, as it can help detect and address underlying vascular abnormalities contributing to the bleeding. This approach is particularly helpful when other methods have proven unsuccessful.

Overall, a multidisciplinary approach that includes appropriate stabilization, pharmacologic therapy, and procedural intervention is essential to effectively manage upper GI bleeding in the pediatric population [12,15,35].

Geriatrics

Upper GI bleeding in elderly patients presents unique challenges due to the high-risk nature of this population and the limitations of existing risk assessment tools. Studies indicate that traditional pre-endoscopic risk scores, such as the Glasgow-Blatchford and AIMS65, often fail to accurately predict outcomes like mortality and hospital stay length in geriatric patients, particularly those aged 82 and older, suggesting a need for age-adjusted scoring systems [36]. Despite these challenges, emergency oesophagogastroduodenoscopy is generally safe for elderly patients, with a high survival rate at 90 days post-procedure, although a significant proportion of OGDs yield normal findings, highlighting the importance of careful patient selection [37]. The management of Upper GI bleeding in the elderly is further complicated by recurrent bleeding, as seen in cases involving peptic ulcer disease, which necessitate a multidisciplinary approach and close monitoring to improve outcomes [38]. Recent efforts to develop novel risk scores tailored for the elderly have shown promise, with a new score incorporating factors like comorbidity index and blood pressure demonstrating good discriminative performance for identifying patients suitable for outpatient management [39].

Pregnant Patients

The causes of upper GI bleeding in pregnant women are similar to those in the general population, including conditions such as esophageal ulcers, gastroesophageal reflux disease, and portal vein thrombosis leading to esophageal varices [40]. Haematemesis, or the vomiting of blood, is a common manifestation of upper GI bleeding and can present as bright red or coffee-ground emesis, indicating bleeding from the upper gastrointestinal tract [1, 40]. In rare cases, UGIB in pregnancy can be caused by gastrointestinal stromal tumors (GISTs), as illustrated by a case where a pregnant woman presented with coffee-ground vomiting and was diagnosed with a bleeding GIST at the stomach cardia [41]. Endoscopy is a critical diagnostic and therapeutic tool for upper GI bleeding, but its use in pregnant women is generally reserved for severe or persistent cases due to potential risks to the mother and fetus [42]. Despite the need for endoscopic evaluation in over 12,000 pregnant women annually in the U.S., research on the safety and outcomes of such procedures remains limited [43]. Therefore, careful consideration of the risks and benefits is essential when managing upper GI bleeding in pregnant patients.

When To Admit This Patient

Admission is required for elderly patients over the age of 60 years, those who require blood transfusions, and patients with a Glasgow-Blatchford Score (GBS) greater than 0 [4,8]. Patients with high-risk bleeding sources should be admitted to a monitored setting or an intensive care unit (ICU) to allow close monitoring for signs of rebleeding and other potential complications.

The decision to discharge a patient following endoscopy depends on the identification of the bleeding source and the associated risk of rebleeding. Patients can be considered for discharge if they meet all of the following criteria: a GBS of 0, blood urea nitrogen (BUN) less than 18 mg/dL, haemoglobin >13 g/dL in men and >12 g/dL in women, heart rate less than 100 beats per minute, systolic blood pressure greater than 110 mmHg, no evidence of melena or syncope since the initial presentation, absence of heart failure or liver failure, and prompt access to outpatient follow-up care.

However, it is important to note that this recommendation is based on low-quality evidence, and clinical judgment should play a significant role in the final decision to discharge a patient. Clinicians should carefully assess each patient’s overall condition, risk of rebleeding, and ability to follow up in an outpatient setting to ensure safe discharge planning [15].

Revisiting Your Patient

In managing this patient, the immediate priority is to assess airway, breathing, and circulation and provide stabilization. Given the patient’s vital instability, they should be promptly transferred to the resuscitation bay for further management.

The image was produced by using ideogram 2.0.

Airway and Breathing: The patient’s airway is currently patent, and they are communicating comfortably, with no signs of obstruction such as pooling of blood or secretions. There have been no further episodes of haematemesis, and the patient is maintaining adequate oxygen saturation on room air. Chest auscultation is clear. At this time, the patient does not require airway adjuncts or intubation, but close observation is essential to detect any deterioration.

Circulation: The patient is hypotensive, indicating the need for immediate intervention. Two large-bore IV cannulas should be inserted to initiate intravenous fluid resuscitation. Crossmatched and uncrossmatched blood should be arranged as a precaution. A point-of-care venous blood gas test must be performed to quickly evaluate acidosis, haemoglobin levels, and other critical parameters. Care should be taken to avoid fluid overload, especially in patients with underlying liver disease.

Further History and Review of Systems: On further evaluation, the patient denies haematochezia, haemoptysis, epistaxis, melena, chest pain, palpitations, syncope, loss of consciousness, or confusion.

Past Medical and Surgical History and Risk Factors: The patient has a history of alcoholic liver disease and is a smoker. There is no history of chronic NSAID use, Helicobacter pylori infection, recent forceful retching, or ingestion of foods or medications that might cause red-colored secretions. There are no known coagulopathies, recent anticoagulant use, vascular abnormalities, weight loss, or loss of appetite. Additionally, the patient has no history of prior surgery.

Examination: Clinical signs of hemodynamic instability, such as hypotension, suggest hypovolemic shock, requiring prompt management with IV fluids and blood transfusion. Examination findings of jaundice, abdominal distension with shifting dullness, and caput medusae are consistent with alcoholic liver disease and indicate probable variceal bleeding. There is no abdominal tenderness, guarding, rigidity, or rebound tenderness to suggest another abdominal pathology.

Laboratory Investigations: Laboratory tests sent include a complete blood count, urea, electrolytes, creatinine, coagulation screen, liver function tests, and type and crossmatch for transfusion. The point-of-care venous blood gas reveals acidosis, haemoglobin <8 g/dL, negative base excess, and elevated lactate, indicating ongoing active bleeding. These findings necessitate urgent gastroenterology consultation for endoscopic intervention and the arrangement of blood transfusion. In addition, the patient must be monitored for liver disease-induced coagulopathy, and a haematology consultation is warranted.

Diagnostic Test: The patient’s Glasgow-Blatchford Score is greater than 0, further confirming the need for urgent endoscopy to identify and control the source of bleeding, which is most likely esophageal varices. Simultaneously, resuscitation measures must continue.

Medications: Given the patient’s history of alcoholic liver disease and suspected variceal bleeding, appropriate pharmacological management should include vasoactive agents such as somatostatin, octreotide, or terlipressin to reduce portal pressure. Empirical antibiotics (fluoroquinolones or third-generation cephalosporins) should be administered to reduce the risk of infection. Additionally, proton pump inhibitors (PPIs) should be started as part of the management protocol.

Disposition: This patient requires urgent gastrointestinal consultation for endoscopy to achieve source control of the bleeding. Admission is necessary to allow for close monitoring of potential complications, including rebleeding and complications of alcoholic liver cirrhosis, such as hepatic encephalopathy and renal failure.

Authors

Picture of Resshme Kannan Sudha

Resshme Kannan Sudha

Resshme Kannan Sudha graduated from RAK Medical and Health Sciences University and is currently an Emergency Medicine Graduate Resident at STMC Hospital, Al Ain. She is a keen follower of FOAMed projects and an enthusiastic educator. Her special interests include critical care, POCUS, global health, toxicology and wilderness medicine.

Picture of Thiagarajan Jaiganesh

Thiagarajan Jaiganesh

STMC Hospital, Al Ain

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References

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  28. Seo YS, Park SY, Kim MY, et al. Lack of difference among terlipressin, somatostatin, and octreotide in the control of acute gastroesophageal variceal hemorrhage. Hepatology. 2014;60(3):962. doi:10.1002/hep.27006
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  30. Fernando T, Donaldson R, Grove G, et al. Metoclopramide. WikEM. Updated March 7, 2021. Accessed April 11, 2023. https://www.wikem.org/wiki/Metoclopramide
  31. Roberts I, Shakur-Still H, Afolabi A, et al. Effects of a high-dose 24-h infusion of tranexamic acid on death and thromboembolic events in patients with acute gastrointestinal bleeding (HALT-IT): an international randomised, double-blind, placebo-controlled trial. Lancet. 2020;395(10241):1927-1936. doi:10.1016/s0140-6736(20)30848-5
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  33. Donaldson R, Gausepohl A, Janeway H, et al. Ciprofloxacin. WikEM. Updated October 17, 2021. Accessed April 11, 2023. https://wikem.org/wiki/Ciprofloxacin
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  35. Lirio RA. Management of upper gastrointestinal bleeding in children. Gastrointest Endosc Clin N Am. 2016;26(1):63-73. doi:10.1016/j.giec.2015.09.003
  36. Di Gioia G, Sangineto M, Paglia A, et al. Limits of pre-endoscopic scoring systems in geriatric patients with upper gastrointestinal bleeding. Sci Rep. 2024;14(1). doi:10.1038/s41598-024-70577-2.
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Reviewed and Edited By

Picture of Arif Alper Cevik, MD, FEMAT, FIFEM

Arif Alper Cevik, MD, FEMAT, FIFEM

Prof Cevik is an Emergency Medicine academician at United Arab Emirates University, interested in international emergency medicine, emergency medicine education, medical education, point of care ultrasound and trauma. He is the founder and director of the International Emergency Medicine Education Project – iem-student.org, chair of the International Federation for Emergency Medicine (IFEM) core curriculum and education committee and board member of the Asian Society for Emergency Medicine and Emirati Board of Emergency Medicine.

Acute Mesenteric Ischaemia (2024)

~ iEM Education Project Team ~ Leave a comment

by Colin NG

Authors
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You have a new patient!

An 80-year-old gentleman presents to our department with a two-day history of abdominal pain accompanied by diarrhea and nausea. He describes the pain as recurrent, having occurred periodically over the past two years, with a crescendo pattern. However, this current episode has not been resolved and is excruciating.

a-photo-of-an-80-year-old-male-patient-(the image was produced by using ideogram 2.0)

A review of his medical records reveals a history of hypertension, dyslipidemia, a previous transient ischemic attack, and atrial fibrillation (AF). He underwent cholecystectomy many years ago for biliary colic. There is no other significant medical history.

On examination, his vital signs are as follows:

  • Blood pressure is 95/57 mmHg.
  • Pulse is 126 beats per minute.
  • Respiratory rate is 26 breaths per minute.
  • Oxygen saturation is 95%.
  • He is afebrile.

The patient appears pale, diaphoretic, and in significant discomfort. There is no clinical jaundice. Abdominal examination reveals diffuse tenderness, most prominent centrally, without guarding. Bowel sounds are sluggish. A cholecystectomy scar is noted in the right hypochondrium. Cardiac examination reveals irregular tachycardia, and the lungs are clear. Examination of the lower limbs is unremarkable, with no swelling. Stool is brown, with no visible blood or melena.

How would you proceed with further evaluation for this patient?

What do you need to know?

Acute mesenteric ischemia (AMI) refers to the sudden loss of blood flow to the small intestine, typically due to arterial insufficiency caused by an embolus or thrombus. AMI falls under the broader category of intestinal ischemia, which includes ischemia of the colon and, more rarely, the stomach and upper gastrointestinal tract. Other forms of intestinal malperfusion include venous occlusion as well as chronic or non-occlusive mesenteric ischemia [1].

Importance

Acute mesenteric ischemia carries an alarmingly high mortality rate, estimated between 60–80%. This is exacerbated by its nonspecific presentation, which often delays diagnosis and increases the likelihood of complications. Early recognition, timely resuscitation and treatment, and prompt advocacy for intervention are essential to improving outcomes [2,3].

Epidemiology

The incidence of AMI in developed countries is approximately 5 per 100,000 people annually, with a prevalence of around 0.1% of all hospital admissions.

AMI primarily occurs in patients with pre-existing atherosclerotic disease of arteries, often associated with risk factors such as advanced age, hypertension, diabetes, and atrial fibrillation [4].

A non-exhaustive list of risk factors includes [1]:

  • Cardiac conditions (e.g., atrial fibrillation, recent myocardial infarction)
  • Aortic surgery or instrumentation
  • Peripheral artery disease
  • Haemodialysis
  • Use of vasoconstrictive medications
  • Prothrombotic disorders
  • Systemic inflammation or infections
  • Hypovolaemic states
  • Bowel strangulation (e.g., volvulus, hernias)
  • Vascular compression syndromes.

Pathophysiology

The intestinal system exhibits relatively low oxygen extraction; residual oxygenated blood from intestinal veins is delivered to the liver via the portal vein. For ischaemic damage to occur, blood flow must be reduced by at least 50% of normal levels [1].

Interestingly, mesenteric arteries are less affected by atherosclerosis compared to other similarly sized vessels, likely due to protective hemodynamic factors. As a result, patients with AMI often have concurrent atherosclerotic conditions elsewhere, such as cerebrovascular disease, ischaemic heart disease, or peripheral vascular disease. Regarding the mechanism,

  • Embolism of the mesenteric artery accounts for ~50% and
  • Thrombosis of the mesenteric artery accounts for ~25% of AMI cases.

Mesenteric venous thrombosis can mimic AMI in a minority of cases, often presenting as nonspecific abdominal pain with diarrhea lasting 1–2 weeks. In some instances, these thrombi resolve spontaneously.

Medical History

The primary symptom of acute mesenteric ischemia (AMI) is central and severe abdominal pain, classically described as being “out of proportion” to physical examination findings. The initial pain is due to visceral ischemia, which initially spares the parietal peritoneum. Peritonism with abdominal rigidity typically develops later, indicating full-thickness ischemia, necrosis, or perforation [5].

Early symptoms may include persistent vomiting and defecation. As the condition progresses, passage of altered blood may occur. Unfortunately, associated gastrointestinal symptoms such as nausea, vomiting, and diarrhea can mimic infective causes, potentially leading to misdiagnosis. While bloody diarrhea is more commonly associated with colonic ischemia, it is less frequent in small bowel ischemia.

In some cases, AMI is preceded by symptoms of chronic non-occlusive mesenteric ischemia. Patients often report recurrent, postprandial abdominal pain resulting from an inability to increase blood flow to meet intestinal vascular demands. This may lead to a fear of eating and significant weight loss. In patients with chronic non-occlusive mesenteric ischemia, symptoms tend to be even more vague. Pain may be less severe and poorly localized, and patients may present with subtle signs such as abdominal distension or occult gastrointestinal bleeding [6].

In addition to embolic causes, mesenteric ischemia can be worsened by systemic conditions that restrict blood flow, such as hemorrhage, hypovolaemia, shock, and low-output cardiac states.

Physical Examination

In the early stages of AMI, physical examination findings are often sparse. The patient will typically appear to be in severe pain without relief, and abdominal tenderness is common. Suspicion should be heightened in frail patients of advanced age who may lack sufficient abdominal musculature to produce guarding during the examination.

Patients may appear pale due to pain or anemia, but specific physical signs are limited in this condition. Diagnosis often relies on a combination of clinical history and thorough investigation.

AMI is a critical condition characterized by reduced blood flow to the intestines, leading to severe complications if not diagnosed early. The physical examination findings should be combined with clinical history and specific symptoms. Understanding these findings is essential for timely intervention.

Key Findings

  • Severe Abdominal Pain: Patients typically present with a sudden onset of severe abdominal pain, which is a hallmark symptom of AMI.
  • Painless Interval: Following the initial pain, a transient painless period may occur, potentially misleading the diagnosis.
  • Signs of Peritonitis: Physical examination may reveal tenderness, guarding, or rebound tenderness, indicating peritoneal irritation and necessitating immediate surgical evaluation.
  • Bowel Sounds: Diminished or absent bowel sounds can suggest intestinal ischemia.

Importance of Clinical History to Guide Physical Exam

  • Risk Factors: A thorough history should include predisposing factors such as cardiovascular disease, recent surgeries, or conditions leading to hypercoagulability.
  • Chronic Symptoms: In cases of arterial thrombosis, patients may report a history of intermittent abdominal pain, weight loss, or diarrhea.

Alternative Diagnoses

The nonspecific symptoms of AMI mean it can be mimicked by many other conditions that are not easily excluded based on history and examination alone. Risk factors such as advanced age, prothrombotic states, atherosclerosis, and conditions causing hypovolaemia should raise clinical suspicion.

Differential diagnoses include:

  • Acute gastroenteritis: Main differential due to similar gastrointestinal symptoms (nausea, diarrhea, vomiting), especially at the initial stages of AMI, but pain and tenderness are typically less severe, more intermittent, and responsive to analgesia. Gastroenteritis is also less likely to cause metabolic acidosis or other significant biochemical abnormalities.
  • Acute cholecystitis: Presents with pain mainly in the right upper quadrant (RUQ) radiating to the right shoulder, often triggered by fatty meals, with accompanying nausea, vomiting, and fever. Murphy’s sign (pain and inspiratory arrest on palpation of the gallbladder) is often positive, particularly in those with a history of gallstones or biliary colic.
  • Acute pancreatitis: Epigastric pain radiating to the back, along with nausea and vomiting, is common. Associated with gallstones or alcohol use. Physical findings include epigastric tenderness, reduced bowel sounds, and, in severe cases, Grey-Turner’s or Cullen’s sign. Diagnosis is supported by elevated serum lipase or amylase levels.
  • Peptic ulcer disease: Characterized by burning or gnawing epigastric pain, often relieved by food or antacids. Common risk factors include NSAID use and Helicobacter pylori infection. Examination is typically unremarkable unless perforation occurs, which may result in acute peritonitis.
  • Bowel perforation: Sudden severe, diffuse abdominal pain with signs of peritonitis (rebound tenderness, guarding), fever, and tachycardia. A history of PUD or diverticulitis may be present. Diagnosis is supported by imaging, showing free air under the diaphragm on X-ray.
  • Diverticulitis: Presents with localized left lower quadrant (LLQ) pain, fever, and altered bowel habits (diarrhea or constipation). LLQ tenderness or a palpable mass is often noted in older patients.
  • Bowel obstruction: Crampy, intermittent abdominal pain, nausea/vomiting, abdominal distension, and constipation, potentially progressing to obstipation. Examination reveals a distended abdomen with high-pitched or absent bowel sounds. Plain X-rays typically show air-fluid levels and dilated bowel loops.
  • Ureteric calculus: Sudden colicky flank pain radiating to the groin, often with hematuria, nausea, and vomiting. A history of kidney stones is common. Findings include costovertebral angle tenderness, with a generally unremarkable abdominal exam. Hematuria is detected on urinalysis.

Acing Diagnostic Testing

Bedside Tests

Bedside diagnostics are limited but can provide valuable clues:

  • ECG: May reveal atrial fibrillation, a common risk factor.
  • Blood glucose: Hyperglycaemia due to physiological stress.
  • Point-of-Care Testing (POCT) for lactate: Elevated levels may indicate tissue hypoxia, though not specific to AMI.
  • Ultrasound: Limited in diagnosing AMI but useful for ruling out other causes of abdominal pain (e.g., cholecystitis, abdominal aneurysm, or ureteric colic). Ultrasound can also assess fluid status and response to fluid resuscitation via the inferior vena cava (IVC) and right heart function, particularly in patients with cardiac or renal comorbidities or failure.
An ECG sample in an abdominal pain patient - Rapid ventricular rate, atrial fibrillation.

Laboratory Tests

No serum markers are sufficiently sensitive or specific to diagnose AMI reliably:

  • Complete blood count (CBC): It may reveal haemoconcentration or leukocytosis but lacks specificity.
  • Serum lactate: Highly sensitive in bowel infarction but nonspecific; elevated levels may not occur in the early stages.

Leucocytosis and elevated lactate levels are the two most frequently observed abnormalities in acute mesenteric ischemia; however, both lack specificity for this condition [7,8].

  • Blood gas analysis: Metabolic acidosis is a late finding; its presence should heighten suspicion in the appropriate clinical context.
  • Serum amylase: Moderately elevated in more than half of cases; highly elevated levels suggest pancreatitis, which should guide further diagnostic steps.

Imaging

  • X-rays (Chest/Abdomen): Chest and abdominal X-rays are often normal in the early stages of acute mesenteric ischemia but are useful for identifying complications or alternative diagnoses (e.g., perforation, ureteric calculus) [9]. Early findings may include adynamic ileus, distended air-filled bowel loops, or bowel wall thickening. Late findings such as pneumatosis or portal venous gas strongly suggest bowel infarction.
  • CT Scanning: The primary imaging modality in diagnosing AMI. When enhanced with contrast, CT can detect bowel wall edema, mesenteric edema, abnormal gas patterns, intramural gas, ascites, and mesenteric venous thrombosis. Sensitivity and specificity are high (82.8–97.6% and 91.2–98.2%, respectively), though contrast use may be limited by renal function [10]. However, delaying diagnosis poses greater risks than the small chance (~1%) of contrast-induced nephropathy requiring dialysis [11].
The CT image shows bowel wall thickness.
  • Catheter Angiography: is considered the gold standard but rarely available in emergency settings [10]. It may still be necessary if CT is inconclusive and clinical suspicion remains high.
  • Diagnostic Laparotomy: it may be required for definitive diagnosis in cases of high suspicion when imaging is non-diagnostic.

Risk Stratification

No validated tools exist for risk stratification in AMI. However, specific features indicate late-stage disease and worse prognosis:

  • Prolonged symptoms before presentation.
  • Evidence of bowel necrosis or perforation.
  • Severe biochemical derangements (e.g., high lactate, metabolic acidosis).
  • Hemodynamic instability, such as septic or hemorrhagic shock.

Management

Initial Stabilization

Initial stabilization of the patient, if required, is straightforward but must follow a systematic approach, following airway, breathing, circulation, disability, and exposure.

Airway and Breathing:

The airway should be secured if necessary, especially in cases where the patient appears drowsy due to cerebral hypoperfusion or septic encephalopathy, or if they are actively vomiting and at high risk of aspiration. Rapid correction of hypovolaemia before administering sedatives or paralytics is recommended. Breathing is not commonly compromised in this condition; however, supplemental oxygen may be required for patients experiencing atelectasis or tachypnoea secondary to pain.

C: Circulation – Circulation management necessitates aggressive and rapid resuscitation with fluids or blood products. Fluid resuscitation should not be delayed due to difficulty in obtaining IV access. Ultrasound guidance can be used if venous access proves challenging. If the patient is hypotensive, an initial 10–20 mL/kg (Crystalloids: Normal saline / Hartmann’s / Ringer’s lactate / Plasmalyte etc.) bolus delivered rapidly over 5–15 minutes is appropriate. This usually requires at least one large-bore IV line (20G or larger).

Many of these patients have comorbidities such as congestive heart failure (CHF), which requires judicious fluid management. Careful hemodynamic monitoring, including repeated clinical assessments and sonographic evaluation of inferior vena cava (IVC) collapsibility, is crucial. If required, more invasive hemodynamic monitoring may be employed.

Vasoactive agents should be avoided due to their role as predisposing factors; however, if vasopressors are essential, it is advisable to avoid alpha-agonist medications.

D: Disability – In patients with acute mesenteric ischemia (AMI), mental status may become altered if ischemia progresses to sepsis or shock, leading to cerebral hypoperfusion. This may present as confusion, agitation, or lethargy. Tools such as the AVPU scale or Glasgow Coma Scale (GCS) are valuable for assessing consciousness and monitoring neurological status during treatment. Clinicians should also consider the presence of sequelae from prior strokes, as these may indicate underlying atherosclerotic disease, which is a risk factor for AMI. Additionally, severe pain can interfere with the patient’s ability to engage fully in the assessment, even when mental status remains intact.

E: Exposure – The patient should be fully exposed to enable a thorough examination, while ensuring measures are taken to maintain warmth and prevent hypothermia, as this can worsen shock. A systematic palpation of the abdomen is critical to identify tenderness, guarding, or masses. In the early stages of AMI, there may be no external signs, but central or generalized abdominal tenderness is typically present. As the condition advances, abdominal distension and signs of peritonitis, such as rebound tenderness and rigidity, may develop.

Clinicians should also observe for secondary indicators, including surgical scars or stomas, which may suggest a history of abdominal pathology. Systemic signs of hypoperfusion and shock, such as mottled skin or cool extremities, should also be noted. Regular and frequent reassessment is essential to detect any progression or subtle changes in the patient’s condition, ensuring timely and appropriate intervention.

Early and empirical administration of broad-spectrum antibiotics is critical and should not be delayed for blood culture collection, as the risk of bacterial translocation across the bowel wall is high. Oral intake must be avoided since these patients are likely to undergo urgent surgery under general anesthesia. Electrolyte imbalances should also be corrected promptly.

Antibiotic Administration

Ceftriaxone

  • Dose per kg: 1–2 g
  • Frequency: Stat (given immediately)
  • Maximum Dose: 2 g
  • Category in Pregnancy: Category B (safe for all trimesters)
  • Cautions/Comments: None specified.

Metronidazole

  • Dose per kg: 500 mg
  • Frequency: Stat (given immediately)
  • Maximum Dose: 500 mg
  • Category in Pregnancy: Category B (safe for all trimesters)
  • Cautions/Comments: None specified.

An urgent surgical consultation is imperative, as acute mesenteric ischemia is a time-sensitive condition. Delays to definitive treatment significantly increase morbidity and mortality. High clinical suspicion alone should prompt surgical involvement, even before imaging results are available. In critically ill patients, surgical teams may decide to proceed directly to the operating theatre without advanced imaging. Such decisions are typically made collaboratively by the emergency department, surgical, anesthetic, and intensive care teams.

The definitive treatment for acute mesenteric ischemia depends on the underlying cause and whether necrotic bowel is present. Necrotic bowel or signs of peritonitis necessitate immediate resection. Specific interventions include embolectomy with distal bypass grafting for mesenteric artery embolism, bypass grafting or stenting for mesenteric artery thrombosis, and removal of underlying stimuli in nonocclusive ischemia, sometimes supplemented with direct transcatheter papaverine infusion. Mesenteric venous thrombosis typically requires anticoagulation [7].

Special Patient Groups

Special populations, such as those with communication barriers or cognitive impairments, may require a lower threshold for advanced imaging since history-taking and physical examination may be unreliable. Pregnant and pediatric patients are rarely affected by this condition.

When To Admit This Patient

Given the critical nature of acute mesenteric ischemia and its high mortality rates, all affected patients should be admitted to the intensive care unit for postoperative management following surgery.

Revisiting Your Patient

Our patient was triaged to a high-acuity area of the emergency department (ED) and placed on continuous monitoring, including cardiac leads, blood pressure, and oximetry. Stabilization proceeded in a structured, prioritized manner, focusing on critical areas from A to E:

  • Airway and Breathing: The patient’s airway was intact, and there were no signs of active vomiting. Mild dyspnoea was reported, so supplemental oxygen was administered via nasal cannula.
  • Circulation: Two large-bore intravenous cannulae were inserted, and a liter of crystalloids was infused. This led to visible hemodynamic improvement, including better IVC collapsibility observed on ultrasound.
  • Disability and Exposure: Disability and exposure did not reveal anything abnormal except for a generalized tenderness on the abdomen.

With the patient stabilized, the team moved on to investigations. Blood samples were taken, including a point-of-care venous gas test with serum lactate, coagulation profile, and a group and cross-match. Leucocytes were elevated at 12,000, and serum lactate was elevated at 8. Cardiac monitoring revealed atrial fibrillation. Bedside ultrasound did not reveal other causes of abdominal pain, such as a ruptured aneurysm or cholecystitis. Chest and abdominal X-rays were normal.

Based on the clinical presentation, risk factors, and lab results, the treating team suspected acute mesenteric ischemia. A surgical consult was requested, and a CT scan of the abdomen and pelvis was ordered. Maintenance IV crystalloids and broad-spectrum antibiotics (ceftriaxone and metronidazole) were started empirically. A urinary catheter was placed to monitor fluid balance.

The CT scan revealed:

  • A thickened small bowel wall with dilated bowel loops
  • An embolism in the superior mesenteric artery

The patient was immediately taken to the operating theatre for definitive treatment.

In summary, the role of the ED physician is to:

  1. Stabilize the patient through targeted resuscitation
  2. Make an early diagnosis based on clinical suspicion supported by available investigations
  3. Understand the limitations of laboratory tests in ruling out acute mesenteric ischemia
  4. Prioritize aggressive resuscitation and management
  5. Ensure urgent surgical involvement

Authors

Picture of Colin NG

Colin NG

Woodlands Health

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References

  1. Tendler DA, Lamont JT. Overview of intestinal ischemia in adults. UpToDate. https://www.uptodate.com/contents/overview-of-intestinal-ischemia-in-adults Updated January 29, 2024. Accessed December 9, 2024.
  2. McKinsey JF, Gewertz BL. Acute mesenteric ischemia. Surg Clin North Am. 1997;77(2):307-318.
  3. Oldenburg WA, Lau LL, Rodenberg TJ, Edmonds HJ, Burger CD. Acute mesenteric ischemia: a clinical review. Arch Intern Med. 2004;164(10):1054-1062.
  4. Szuba A, Gosk-Bierska I, Hallett RL. Thromboembolism. In: Rubin GD, Rofsky NM, ed. CT and MR Angiography: Comprehensive Vascular Assessment. Philadelphia, PA, USA: Lippincott Williams & Wilkins; 2009: 295-328.
  5. Marc Christopher Winslet. Intestinal Obstruction. In: R.C.G. Russell ed. Bailey & Love’s Short Practice Of Surgery 24th ed. London, UK: Arnold; 2004:1202.
  6. Tendler DA, Lamont JT. Nonocclusive mesenteric ischemia. UpToDate. https://www.uptodate.com/contents/nonocclusive-mesenteric-ischemia Updated December 13, 2023. Accessed December 9, 2024.
  7. Park WM, Gloviczki P, Cherry KJ Jr, et al. Contemporary management of acute mesenteric ischemia: Factors associated with survival. J Vasc Surg. 2002;35(3):445-452.
  8. Cudnik MT, Darbha S, Jones J, Macedo J, Stockton SW, Hiestand BC. The diagnosis of acute mesenteric ischemia: A systematic review and meta-analysis. Acad Emerg Med. 2013;20(11):1087-1100.
  9. Smerud MJ, Johnson CD, Stephens DH. Diagnosis of bowel infarction: a comparison of plain films and CT scans in 23 cases. AJR Am J Roentgenol. 1990;154(1):99-103.
  10. Menke J. Diagnostic accuracy of multidetector CT in acute mesenteric ischemia: systematic review and meta-analysis. Radiology. 2010;256(1):93-101.
  11. Mehran R, Aymong ED, Nikolsky E, et al. A simple risk score for prediction of contrast-induced nephropathy after percutaneous coronary intervention: development and initial validation. J Am Coll Cardiol. 2004;44(7):1393-1399.

FOAM and Further Reading

CDEM Curriculum – Patel S, Mesenteric Ischemia – June 2018, https://cdemcurriculum.com/mesenteric-ischemia/ Accessed May 2023

EMdocs – Seth Lotterman. Mesenteric Ischemia: A Power Review. Nov 2014. http://www.emdocs.net/mesenteric-ischemia-power-review/ Accessed May 2023

Reviewed and Edited By

Picture of Elif Dilek Cakal, MD, MMed

Elif Dilek Cakal, MD, MMed

Picture of Arif Alper Cevik, MD, FEMAT, FIFEM

Arif Alper Cevik, MD, FEMAT, FIFEM

Prof Cevik is an Emergency Medicine academician at United Arab Emirates University, interested in international emergency medicine, emergency medicine education, medical education, point of care ultrasound and trauma. He is the founder and director of the International Emergency Medicine Education Project – iem-student.org, chair of the International Federation for Emergency Medicine (IFEM) core curriculum and education committee and board member of the Asian Society for Emergency Medicine and Emirati Board of Emergency Medicine.

Intraosseous (IO) Lines/Access (2024)

~ iEM Education Project Team ~ Leave a comment

by Yousif Al-Khafaji & Mustak Dukandar

Authors
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Introduction

Obtaining intravascular access in the emergency department is one of the most essential steps in managing critically ill patients. While it is a simple step for most patients, it can be the most challenging procedure during resuscitation. The pediatric population has more body fat, making it difficult to localize their veins. In addition, they have tiny peripheral veins that easily collapse in states of shock. On the other hand, in adults, patients who are obese, those who suffer from extensive burns, or are in shock challenge the clinician in obtaining vascular access [1].

Intraosseous (IO) access involves inserting a hollow needle through the cortex of the bone and into the medullary space. This allows clinicians to infuse fluids, medication, or almost anything that can be administered through the intravenous (IV) route and achieve the same desired effect as the IV route. The IO line is merely a bridging tool to buy the clinician time to obtain IV access. In most cases, IO access is a simple procedure, and clinicians should not hesitate to insert an IO line if peripheral IV access attempts fail.

IO lines can safely remain in place for up to 24 hours and are often a bridge to either IV or Central Venous line placement.

Indications

There are clear indications for IO access. Each of these indications highlights the critical role of IO lines in emergency medicine, providing a swift and effective solution for vascular access in life-threatening situations [3]. When IV access cannot be achieved, IO access is safe, reliable, and quick. It can be accomplished in 30 to 60 seconds and even faster with an IO gun. This is especially helpful in pediatric emergencies when time is critical. 

Emergency intravascular access when other methods have failed
IO access is indicated when IV access is not achievable in critical situations, such as trauma, shock, or severe dehydration. In critically ill patients, a maximum of two failed attempts is generally considered sufficient to shift to IO access. The IO line provides a rapid and reliable alternative to IV lines for administering fluids, medications, or blood products directly into the vascular system via the bone marrow [4]. 

Cardiac arrest
During cardiac arrest, time is critical, and establishing vascular access can be challenging. IO access is often used to administer life-saving medications like epinephrine when IV access cannot be obtained quickly. It ensures the rapid delivery of drugs into circulation during resuscitation [5].

Obtaining blood for laboratory evaluation
IO access allows for the collection of blood samples for laboratory testing, including complete blood count, electrolytes, and blood gas analysis [6]. This is especially useful in emergency situations where traditional venipuncture is impractical or impossible.

Contraindications

Physicians should be aware of a couple of important complications. These contraindications emphasize the importance of careful site selection and patient evaluation before performing IO access to minimize complications and maximize the effectiveness of the procedure [1].

Fractured bone
A fracture at the intended site of IO access is an absolute contraindication. Using a fractured bone for IO infusion can result in extravasation of fluids and medications, potentially worsening the injury and causing further complications.

Infection or burn overlaying insertion site
Localized infection or burns at the insertion site pose a significant risk of introducing pathogens into the bone marrow, leading to osteomyelitis or systemic infection. These conditions are absolute contraindications for IO placement.

Prior use of the same bone for IO infusion
Repeated use of the same bone for IO access can damage the bone marrow and structure, increasing the risk of complications such as extravasation or impaired drug delivery. A different site should be chosen for subsequent IO insertions.

Osteoporosis and osteogenesis imperfecta
These conditions result in fragile bones, increasing the likelihood of fractures or other complications during needle insertion. Alternative access methods should be considered for patients with these conditions.

Administration of ultra-short-acting medications like adenosine (relative contraindication)
Medications like adenosine, which rely on rapid systemic distribution, may not be as effective when administered via IO access due to potential delayed uptake into circulation. This is a relative contraindication, depending on the clinical scenario.

Equipment and Patient Preparation

Equipment

IO Needle

  • Ranges from 15-18 gauge needles
  • Color coding is common:
    • Pink (15 mm): For patients weighing 3–39 kg
    • Blue (25 mm): For patients ≥3 kg and above
    • Yellow (45 mm): For patients ≥40 kg, excessive tissue, or dense bone sites (e.g., proximal humerus or anterior superior iliac spine)

IO Devices (to facilitate insertion)

  • Powered IO Drills (e.g., EZ-IO)
  • Manual IO Drills (e.g., Cook IO Needle or Jamshidi-type needle)

Skin Disinfectants

  • Chloraprep
  • Alcohol swabs
  • Optional: Povidine or Chlorhexidine

Syringe and Flush Materials

  • Saline flush (crystalloid solution, e.g., normal saline or lactated Ringer’s)
  • Intravenous tubing

Lidocaine 2% (without epinephrine)

  • For topical and subcutaneous infiltration in awake patients, as they may experience pain during fluid infusion rather than needle insertion.

Additional Equipment

  • Infusion pump (to regulate fluid delivery)
  • Tape (for securing the IO line)
Arrow® EZ-IO® Intraosseous Vascular Access System - adopted from https://www.teleflex.com/usa/en/product-areas/emergency-medicine/intraosseous-access/arrow-ez-io-system/use-and-application/Arrow_EZ-IO_Landmarking_Poster.pdf

Patient Preparation

  1. Informed Consent
    • Obtain informed consent by explaining the procedure, its benefits, and associated risks to the patient or their guardians. In emergency situations where consent cannot be obtained, implied consent applies.
  2. Site Selection
    • Choose the most appropriate insertion site based on the clinical scenario. Common sites include:
      • Humeral Head
      • Proximal Tibia
      • Medial Malleolus
      • Sternum
      • Distal Radius
      • Distal Femur
      • Anterior Superior Iliac Spine
    • Note: The proximal tibia and humeral head are most commonly used during cardiac arrest as these locations do not interfere with other life-saving procedures like intubation [7].
  3. Contraindication Assessment
    • Ensure there are no contraindications (e.g., fractures, infections, burns, prior IO use at the same site, or certain bone conditions) at the intended site of insertion.
  4. Site Exposure
    • Properly expose the selected insertion site to facilitate accurate placement and reduce the risk of contamination.
  5. Universal Precautions
    • Apply universal precautions, such as wearing gloves at a minimum, to maintain aseptic conditions during the procedure.
  •  
IO placement locations. IO size (color) is subject to the patients body weight.

Sites of IO insertion and some hints [8]

  1. Proximal Tibia
    • 2 finger breadths below the tibial tuberosity (1-3 cm) on the medial, flat aspect of the tibia.
    • Commonly used for ease of access, especially in emergencies.
  2. Distal Tibia
    • Medial surface at the junction of the medial malleolus and the shaft of the tibia, posterior to the greater saphenous vein.
  3. Proximal Humerus (Adults only; use the yellow needle)
    •  Preparation:
      • Keep the arm adducted and internally rotated (rest the patient’s hand on their bellybutton).
      • Slide fingers up the humerus until you feel the notch (surgical neck).
    •  Insertion:
      • Insert the IO needle 1 cm above the surgical neck into the greater tubercle.
      • Immobilize the arm to prevent displacement of the IO line (avoid shoulder abduction).
  4. Distal Femur
    • Primarily used in infants and children due to easier bone access and growth plate considerations.
  5. Pelvic Anterior Superior Iliac Spine (ASIS)
    • An alternative site, especially when lower extremity or upper extremity sites are unavailable.
  6. Sternum
    • Provides the highest flow rate of any location, making it suitable for rapid infusions during critical situations.

Procedure Steps

  1. Preparation
    • Identify the designated site using a sterile gloved finger.
    • Disinfect the overlying skin using appropriate antiseptic (e.g., chlorhexidine).
    • Administer local anesthetic if the patient is awake.
    • Ensure the stylet is properly positioned on the needle prior to insertion.
    • Prepare necessary equipment, including a 20 ml saline syringe, IV tubing, tape, medications, fluids, and infusion pump.
  2. Needle Insertion
    • Insert the needle perpendicularly through the skin down to the bone.
    • Use an IO drill or manually twist the needle clockwise with firm, gentle pressure until a “give” is felt (loss of resistance), indicating entry into the marrow.
    • Ensure the needle locks into place.
  3. Confirmation of Placement
    • The needle should stand upright without additional support if properly positioned.
    • Remove the stylet and attach a syringe.
    • Aspirate to confirm the presence of marrow or blood (not always visible).
    • Gently flush the line with saline while observing for swelling at or around the insertion site.
  4. Troubleshooting
    • If swelling occurs or the test injection fails, remove the IO needle and repeat the procedure on a different site.
  5. Securing and Using the IO Line
    • If Io works properly, stabilize the needle using tape or gauze padding as necessary.
    • Attach IV tubing to the needle hub.
    • Begin infusion of fluids, blood products, or medications.
    • If the patient is awake and experiences pain during infusion, administer lidocaine through the IO line for analgesia [2].
  •  

Complications [9]

Extravasation of Fluid

Occurs when fluid or medication leaks into surrounding soft tissues instead of the bone marrow cavity. This can cause localized swelling, tissue damage, and discomfort. Proper placement and observation for swelling during infusion are essential to avoid this complication.

Compartment Syndrome

Results from increased pressure within a muscle compartment due to extravasation of fluid. It can compromise blood flow, leading to tissue ischemia and potential necrosis. Immediate recognition and corrective action are necessary to prevent long-term damage [10].

Bone Fracture

More common in patients with pre-existing bone disorders, such as osteoporosis or osteogenesis imperfecta. Improper needle insertion technique can increase the risk of fracturing the bone at the insertion site. Physicians should be careful when inserting IO lines in small children because too much pressure during drilling may cause fractures.

Osteomyelitis

A rare but serious complication involving infection of the bone and marrow. This risk increases if aseptic technique is not followed or if there is a pre-existing infection near the insertion site.

Preventative Measures:

  • Use strict aseptic technique to minimize infection risks.
  • Properly assess the patient’s bone health and contraindications before insertion.
  • Monitor the insertion site for early signs of complications, such as swelling or pain, during and after infusion

Hints and Pitfalls

Purpose and Time Limit

  • IO access is a bridging tool used to buy time for obtaining peripheral or central IV access.
  • IO needles should not remain in place for more than 24 hours, as the risk of complications increases significantly after that time frame.

Site and Device Selection

  • Always use an uninjured limb for IO placement; if no uninjured limb is available, the sternum is preferred.
  • An IO drill or gun is recommended over manual insertion for consistent and reliable placement.
  • Needle selection must be appropriate for the selected site and the marrow cavity to ensure proper access.

Needle Placement and Security

  • IO needle displacement can sometimes occur, especially in pediatric patients with soft bones; this can be mitigated by securing the needle to the skin properly.
  • The anterior superior iliac spine may be considered as an alternative site in cases of soft bone structures.

Medication and Dosage

  • Any medication that can be administered via IV access can also be given through IO access without dose adjustment, as the bioequivalence between IO and IV routes is similar. [11,12]

Laboratory Sampling

  • Lab tests with good correlation from IO samples include hemoglobin/hematocrit, chloride, glucose, urea, creatinine, and albumin.
  • Other lab values, such as WBC, platelets, serum CO2, sodium, potassium, and calcium, may not correlate well with venous samples. [13]
  •  

Special Patient Groups

Pediatrics

  • Challenges: In pediatric patients, the bones can sometimes be too soft, which increases the risk of needle displacement even when placed correctly.
  • Recommendation: To mitigate this risk, consider using the anterior superior iliac spine as an alternative site. This site may provide a more stable placement in cases where traditional sites like the tibia are less effective.

Geriatrics

  • Challenges: Older adults often have pre-existing bone disorders such as osteoporosis, which make their bones more fragile.
  • Risks: IO insertion in such patients can lead to fractures, especially if not performed with careful technique and appropriate needle selection.
  • Recommendation: Perform a thorough assessment of bone health and use alternative vascular access methods if significant bone fragility is present.

Pregnant Patients

  • Considerations: There are no contraindications for IO insertion in pregnant women. This makes IO access a viable option during emergencies where quick vascular access is necessary.
  • Precautions: Ensure that the chosen site does not interfere with obstetric care and consider patient positioning to maintain comfort and safety during the procedure.

Authors

Picture of Yousif Al-Khafaji

Yousif Al-Khafaji

Chief Emergency Medicine Resident - Tawam Hospital, Al Ain, UAE

Picture of Mustak Dukandar

Mustak Dukandar

Tawam Hospital Emergency Department

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References

  1. Roberts and Hedges’ Clinical Procedures in Emergency Medicine and Acute Car-Elsevier (2017), chapter 25
  2. ATLS Student course manual Tenth Edition (2018). Appendix G, 351
  3. Phillips L, Brown L, Campbell T, et al. Recommendations for the use of intraosseous vascular access for emergent and nonemergent situations in various healthcare settings: a consensus paper. J Emerg Nurs. 2010;36(6):551-556. doi:10.1016/j.jen.2010.09.001
  4. Oksan D, Ayfer K. Powered intraosseous device (EZ-IO) for critically ill patients. Indian Pediatr. 2013;50(7):689-691. doi:10.1007/s13312-013-0192-z
  5. Leidel BA, Kirchhoff C, Bogner V, et al. Is the intraosseous access route fast and efficacious compared to conventional central venous catheterization in adult patients under resuscitation in the emergency department? A prospective observational pilot study. Patient Saf Surg. 2009;3(1):24. Published 2009 Oct 8. doi:10.1186/1754-9493-3-24
  6. Tallman CI, Darracq M, Young M. Analysis of intraosseous blood samples using an EPOC point of care analyzer during resuscitation. Am J Emerg Med. 2017;35(3):499-501. doi:10.1016/j.ajem.2016.12.005
  7. Wampler D, Schwartz D, Shumaker J, Bolleter S, Beckett R, Manifold C. Paramedics successfully perform humeral EZ-IO intraosseous access in adult out-of-hospital cardiac arrest patients. Am J Emerg Med. 2012;30(7):1095-1099. doi:10.1016/j.ajem.2011.07.010
  8. Day MW. Intraosseous devices for intravascular access in adult trauma patients. Crit Care Nurse. 2011;31(2):76-90. doi:10.4037/ccn2011615
  9. ACLS provider Manual Supplementary Material (2016). Intraosseous Access, 57-61
  10. Vidal R, Kissoon N, Gayle M. Compartment syndrome following intraosseous infusion. Pediatrics. 1993;91(6):1201-1202.
  11. Faga, M., & Wolfe, B. (2016). Vascular access in hospitalized patients. Hospital Medicine Clinics, 5(1), 1-16.
  12. Von Hoff, D.D., Kuhn, J.G., Burris, H.A. 3rd, & Miller, L.J. (2008). Does intraosseous equal intravenous? A pharmacokinetic study. Am J Emerg Med, 26, 31-38
  13. Miller LJ, Philbeck TE, Montez D, Spadaccini CJ. A new study of intraosseous blood for laboratory analysis. Arch Pathol Lab Med. 2010;134(9):1253-1260.

FOAM and Further Reading

Reviewed and Edited By

Picture of Arif Alper Cevik, MD, FEMAT, FIFEM

Arif Alper Cevik, MD, FEMAT, FIFEM

Prof Cevik is an Emergency Medicine academician at United Arab Emirates University, interested in international emergency medicine, emergency medicine education, medical education, point of care ultrasound and trauma. He is the founder and director of the International Emergency Medicine Education Project – iem-student.org, chair of the International Federation for Emergency Medicine (IFEM) core curriculum and education committee and board member of the Asian Society for Emergency Medicine and Emirati Board of Emergency Medicine.

Fundamentals of Pediatric Advanced Life Support (2024)

~ iEM Education Project Team ~ Leave a comment

by Burak Çakar & Ayça Koca

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Introduction

Pediatric cardiac arrest (CA) is a rare but critical event associated with high mortality and significant risk of severe sequelae [1,2]. Unlike in adults, respiratory causes are the primary contributors to CA in children. Hypoxia and bradycardia can lead to cardiopulmonary failure, which may ultimately progress to CA.

Common causes of pediatric CA include infections (e.g., pneumonia, sepsis), trauma, asphyxia, seizures, asthma, suffocation, and sudden infant death syndrome [2]. Clinical signs of cardiopulmonary arrest include respiratory arrest, absence of a palpable pulse, muscle flaccidity, unresponsiveness, cyanosis or other discoloration, and dilated pupils. Recognizing and promptly addressing these signs is crucial for improving outcomes.

Recognition of a Critically Ill Child

Early recognition of a critically ill child is essential to implementing timely interventions that may prevent progression to CA [3]. Abnormal vital signs, relative to age-specific norms, are often the most reliable indicators of impending arrest.

Pediatric Early Warning Scores (PEWS) are recommended as a systematic tool to identify children at risk of clinical deterioration [4]. PEWS evaluates three domains: behavior, cardiovascular function, and respiratory status [5]. It incorporates vital findings such as respiratory rate, heart rate, blood pressure, oxygen saturation, temperature, level of consciousness, and capillary refill time [6]. 

Monitoring Vital Signs in Children

It is essential to recognize abnormal vital signs for early recognition of pediatric deterioration.

Blood Pressure

Systolic Hypotension is defined as a systolic blood pressure below the 5th percentile for age. The threshold for concern is when the systolic blood pressure is <70 mmHg + (2x the child’s age in years).

Respiratory Rate

Tachypnea: A respiratory rate exceeding 60 breaths per minute indicates tachypnea.
Decreased Respiratory Rate: A reduction in respiratory rate in a previously tachypneic patient could signal either improvement or fatigue. Fatigue in this context could precede respiratory failure, particularly if it occurs in conjunction with other signs of decompensation.

Temperature

Fever significantly affects physiology. For every 1°C increase in body temperature:

  • The heart rate increases by approximately 10 beats per minute.
  • The respiratory rate increases by 2 to 5 breaths per minute.

End-Tidal Carbon Dioxide (EtCO2)

Changes in EtCO2 levels are critical indicators of respiratory status. A progressive increase or decrease in EtCO2 levels can signal impending desaturation and respiratory failure.

Assessment

Given the poor outcomes associated with pediatric CA, the emphasis must be on early recognition of pre-arrest states. Identifying signs of impending respiratory failure and shock, regardless of their underlying cause, should be a primary focus [4].

Findings Preceding Cardiopulmonary Arrest

Key findings preceding cardiopulmonary arrest are categorized as follows:

  1. Airway: Signs include stridor, drooling, and retractions, which indicate significant airway obstruction or distress.

  2. Breathing: Irregular respiration, bradypnea, gasping respirations, and cyanosis are warning signs of severe respiratory compromise.

  3. Circulation: Indicators such as a capillary refill time greater than 5 seconds, bradycardia, hypotension, cool extremities, weak central pulses, and the absence of peripheral pulses suggest circulatory failure.

  4. Disability: An altered level of consciousness and decreased responsiveness point toward significant neurological impairment, often accompanying or preceding arrest.

Initial Assessment

The initial assessment begins with a first impression of the child’s general appearance, breathing pattern, and circulatory status. During the primary assessment, the ABCDE approach is followed, with immediate interventions performed at each step when abnormalities are identified. Initial management focuses on supporting airway, breathing, and circulation [7].

The clinician should rapidly assess the following:

Airway

  • Assess for patency (open, requiring maneuvers/adjuncts, partially or completely obstructed)
  • Perform cervical spine stabilization for injured children.
  • Provide 100% inspired oxygen, clear the airway (e.g., suction), apply airway maneuvers, and insert airway adjuncts if the child is unconscious.
  • Initiate chest compressions immediately if the child is unresponsive and shows no signs of life.
  •  

 Breathing

  • Evaluate respiratory rate, effort, tidal volume, lung sounds, and pulse oximetry.
  • Assist ventilation manually for patients unresponsive to basic airway maneuvers or exhibiting inadequate respiratory effort.
  • Monitor oxygenation and ventilation using pulse oximetry and ETCO₂.
  • Administer appropriate medications based on the cause of respiratory distress (e.g., albuterol for status asthmaticus, inhaled racemic epinephrine for croup).
  • Consider intubation when necessary, ensuring 100% oxygen delivery via a non-rebreather mask. Apply positive pressure ventilation with a bag-valve-mask (BVM) in cases of respiratory failure.

Circulation

  • Assess skin color and temperature, heart rate and rhythm, blood pressure, peripheral and central pulses, and capillary refill time.
  • Control hemorrhage in injured children.
  • For circulation deficiencies, monitor heart rate and rhythm, and establish vascular access for volume resuscitation or medication administration.

Disability

  • Evaluate neurological status and level of consciousness using the AVPU scale (Alert, Voice, Pain, Unresponsive) and the Glasgow Coma Scale (GCS) for trauma patients.
  • Assess pupil size and reactivity to light.
  • Check for hypoglycemia using rapid bedside glucose testing or by observing the response to empiric dextrose administration.

Exposure

  • Examine for skin findings, fever or hypothermia, and evidence of trauma.

Secondary and Tertiary Assessments

  • The secondary assessment involves a detailed head-to-toe physical examination, supplemented with a medical history.
  • The tertiary assessment focuses on identifying the underlying causes of trauma, illness, or infection through ancillary studies.

Respiratory Distress and Failure

Respiratory distress and failure are common precursors to CA in children. Early recognition of breathing difficulties is essential to improving clinical outcomes.

Respiratory distress is characterized by tachypnea, nasal flaring, retractions, and the use of accessory muscles. Additional signs include agitation, hypoxia, and abnormal breath sounds, such as stridor or wheezing. If not promptly addressed, these findings can progress to a decreased respiratory rate, respiratory fatigue, and eventual respiratory arrest.

Bradycardia

In children, bradycardia is often secondary to hypoxia. A heart rate slower than the age-appropriate normal range is indicative of bradyarrhythmia. Management focuses on optimizing oxygenation and ventilation through basic airway maneuvers.

If the heart rate remains below 60 beats per minute despite adequate oxygenation and ventilation, chest compressions should be initiated. Epinephrine (0.01 mg/kg) should be administered every 3–5 minutes. For bradycardia caused by increased vagal tone or primary atrioventricular block, atropine (0.02 mg/kg; maximum single dose 0.5 mg) is recommended [7].

Tachycardia

Tachycardia refers to a heart rate that exceeds the normal range for a child’s age, considering other factors such as physical activity or fever. The management of tachycardias depends on the child’s hemodynamic condition and rhythm [7].

Pulseless Arrest

Pediatric CAs are typically the result of cardiopulmonary distress, failure, or shock. When a child has no palpable pulse and is unresponsive, cardiopulmonary resuscitation (CPR) should be initiated.

A child with pulseless arrest will present as apneic and may exhibit gasping respirations. The rhythms associated with pulseless arrest include [2]:

Shockable rhythms: Ventricular fibrillation (VF), pulseless ventricular tachycardia (pVT).

Ventricular Fibrillation

Ventricular Tachycardia

Unshockable rhythms: Asystole, pulseless electrical activity (PEA).

Asystole

Pulseless Electrical Activity (PEA)

During CPR, reversible causes of PEA should be actively identified and addressed. The mnemonic 6H5T is useful for recalling these potential causes [2]:

  • 6 H’s:
    • Hydrogen ion (acidosis)
    • Hypoxia
    • Hypovolemia
    • Hypo- or hyper -kalemia, -calcemia, -magnesemia
    • Hypoglycemia
    • Hypo- or hyperthermia
  • 5 T’s:
    • Tension pneumothorax
    • Tamponade
    • Thrombosis (cardiac)
    • Thrombosis (pulmonary)
    • Toxic agents

By addressing these potential causes, advanced life support providers can significantly improve the likelihood of successful resuscitation.

Resuscitation

An effective resuscitation team is critical to the successful management of pediatric advanced life support (PALS). The team must perform multiple tasks simultaneously, including airway management, ventilation, vascular access, medication preparation and administration, chest compressions, monitor/defibrillator operation, recording/timing, and overall leadership.

The team leader plays a pivotal role by assigning tasks, directing team members, and modeling exemplary teamwork. In addition to medical expertise and resuscitation skills, the team must demonstrate effective communication. Key elements of effective team dynamics include:

  • Closed-loop communication
  • Clear messages
  • Defined roles and responsibilities
  • Knowing and communicating one’s limitations
  • Knowledge sharing
  • Constructive interventions
  • Reevaluation and summarization
  • Mutual respect [8]

Initiation of CPR

Timely recognition of CA, prompt initiation of high-quality chest compressions, and ensuring adequate ventilation are crucial for improving outcomes [2].

Healthcare providers should begin chest compressions promptly in any child who is unresponsive, not breathing normally, and has no signs of circulation [7, 9]. Pulse checks may be performed but should not delay the initiation of CPR for more than 10 seconds [10, 11]. Pulse palpation alone is unreliable in determining the need for compressions or confirming CA.

Since respiratory-related CA is more common in infants and children than primary cardiac causes, ensuring adequate ventilation during resuscitation is essential [2]. The recommended sequence for CPR is compressions-airway-breathing (CAB) [12].

High-quality CPR enhances blood flow to vital organs and increases the likelihood of return of spontaneous circulation (ROSC). The five key components of high-quality CPR are [2, 13]:

  • Optimal chest compression rate
  • Sufficient chest compression depth
  • Minimal interruptions in compressions
  • Complete chest recoil between compressions [7, 14]
  • Avoidance of excessive ventilation

Components of High-Quality CPR

  • Compression Rate: 100–120 compressions per minute [15–18].
  • Compression Depth:
    • At least one-third of the anterior-posterior diameter of the chest:
      • 4 cm for infants
      • 5 cm for children
      • 5–6 cm for adolescents who have reached puberty [7, 19].
    • Allow complete chest recoil after each compression.
    • Use 100% oxygen with a bag-valve-mask (BVM) during CPR.
    • Compression-Ventilation Ratios:
      • 30:2 for single rescuers.
      • 15:2 for two rescuers [7, 20].

To prevent fatigue and ensure adequate compressions, switch the person performing compressions at least every 2 minutes or sooner if necessary [7].

CPR Technique

For Infants

Single Rescuer: Use two fingers (Figure 1) or two thumbs below the nipple line (lower half of the sternum but one-finger width above the xiphisternum) [21–24].

Figure 1. Two-finger compressions

Two Rescuers: Use the two-thumb encircling hands technique (Figure 2) [25–29].

Figure 2. Thumb-encircling hands compression

If the recommended depth cannot be achieved, use the heel of one hand (Figure 3) [2, 18, 30, 31].

Figure 3. Compression with the heel of one hand

For children older than 1 year

Use either one-handed or two-handed CPR.

Perform chest compressions on a firm surface. Use a backboard or activate the bed’s “CPR mode” if available [32–35].

The Airway

Unless a cervical spine injury is suspected, the head tilt-chin lift maneuver is recommended to open the airway [36]. In trauma patients with suspected cervical spinal injury, the jaw thrust maneuver should be used. If the jaw thrust is ineffective, the head tilt-chin lift may be performed, even in cases of suspected cervical spine injury [2].

Use 100% oxygen delivered via bag-valve-mask (BVM) during CPR.

Advanced Airway Interventions During CPR

Bag-mask ventilation (BMV) is effective for most patients but requires pauses in chest compressions and carries risks of aspiration and barotrauma [2]. Advanced airway interventions, such as supraglottic airway (SGA) placement or endotracheal intubation (ETI), improve ventilation, reduce aspiration risks, and enable uninterrupted chest compressions. However, these procedures require specialized equipment and trained providers, and may be challenging for those inexperienced in pediatric intubation [2]. BMV is more reliable than advanced airway interventions during out-of-hospital pediatric CA [37–39].

For patients with advanced airway, ventilations should be asynchronous. Exceeding recommended ventilation rates can compromise hemodynamics and lower systolic blood pressure [40].

Ventilations should be tailored to age:

  • 25 breaths/min (infants)
  • 20 breaths/min (>1 year)
  • 15 breaths/min (>8 years)
  • 10 breaths/min (>12 years) [7].

Capnography should be used to confirm endotracheal tube placement and monitor for ROSC. However, ETCO₂ should not be used as a definitive quality indicator or target during PALS [7].

Drug Administration During CPR

Establish IV access as early as possible during PALS. If IV access is challenging, promptly consider intraosseous (IO) access as an alternative [7]. Drug dosing for children is typically based on weight, which can be challenging to determine in emergencies. When the actual weight cannot be obtained, various estimation methods are available [41]

The administration of vasoactive agents during CA aims to improve coronary and cerebral perfusion and increase the likelihood of ROSC. However, optimal timing and overall impact on long-term outcomes are still under investigation [42]

  • Administer epinephrine (10 mcg/kg; max 1 mg; IV or IO ) as soon as possible for non-shockable rhythms. For shockable rhythms, administer epinephrine immediately after the third shock, along with antiarrhythmic drugs. Once given, adrenaline should be repeated every 3–5 minutes until ROSC.

Antiarrhythmic drugs can reduce the risk of recurrent VF or pVT and improve the likelihood of successful defibrillation [43, 44]. Only in shockable rhythms, administer antiarrhythmic drugs immediately after the third shock, along with epinephrine.

  • Amiodarone: 5 mg/kg (max 300 mg); a second dose (max 150 mg) may follow after the fifth shock if the rhythm remains shockable.
  • Lidocaine: 1 mg/kg, as an alternative to amiodarone.

Magnesium sulfate (25–50 mg/kg) should be considered for torsades de pointes. Routine administration of sodium bicarbonate and calcium is not recommended unless specific conditions (e.g., electrolyte imbalances, drug toxicities) are present [45–48].

Flush all IV or IO resuscitation drugs with 5–10 mL of normal saline to ensure delivery to the central circulation.

Defibrillation During PALS

Shockable rhythms in children include pulseless ventricular tachycardia (pVT) and ventricular fibrillation (VF). When identified, defibrillation should be performed immediately, regardless of the ECG amplitude. If there is uncertainty about the rhythm, it should be treated as shockable to avoid delays in care. [7].

The preferred method for defibrillation during pediatric ALS is manual defibrillation, but an automated external defibrillator (AED) can be used if manual defibrillation is unavailable. Currently, self-adhesive defibrillation pads are the standard. When using these pads:

  • Chest compressionsshould continue while the defibrillator charges.
  • The pads should be placed in either the antero-lateral (AL)or antero-posterior (AP) positions:
    • AL position: One pad below the right clavicle and the other in the left axilla.
    • AP position: The front pad in the mid-chest just left of the sternum, and the back pad between the scapulae.

Avoid contact between the pads to prevent electrical arcing.

If self-adhesive pads are unavailable, paddles with gel or pre-shaped gel pads can be used as an alternative. In this case, charging should occur directly on the chest, pausing compressions during the process [7]. Pre-planning each step is critical to minimizing delays during the intervention.

Charge the defibrillator for an initial shock of 4J/kg. Avoid exceeding the maximum doses recommended for adults (typically 120–200J, depending on the defibrillator). Pause chest compressions briefly to deliver the shock, ensuring all rescuers are clear of the patient. Resume CPR immediately after the shock, minimizing the pause to under 5 seconds. Reassess the rhythm every 2 minutes and, if it remains shockable, deliver subsequent shocks at 4J/kg. For refractory VF/pVT (requiring more than 5 shocks), incrementally increase the dose up to 8J/kg (maximum 360J) [7].

CPR should continue until an organized, potentially perfusing rhythm is recognized during a rhythm check and is accompanied by signs of ROSC, identified either clinically (e.g., eye-opening, movement, normal breathing) or through monitoring (e.g., etCO2, SpO2, blood pressure, ultrasound) [7].

A summary of the fundamentals of pediatric ALS can be found in Figure 5.

Figure 5. Pediatric cardiac arrest algorithm [7] CPR: cardiopulmonary resuscitation, EMS: emergency medical services, ALS: advanced life support, VF: ventricular fibrillation, pVT: pulseless ventricular tachycardia, PEA: pulseless electrical activity, IV: intravenous, IO: intraosseous.

Post-cardiac Arrest Management

Achieving ROSC is only the first step in resuscitation. Comprehensive post-CA care is crucial to optimizing outcomes, particularly in pediatric patients. This phase focuses on treating the underlying cause of the event and preventing secondary injuries.

Key Components of Post-Cardiac Arrest Care

Targeted Temperature Management (TTM):

  • For unconscious children after ROSC, TTM helps prevent further brain injury.

Ventilation and Oxygenation:

  • Inspired oxygen should be titrated to maintain oxygen saturation (SpO₂) between 94% and 99%.
  • For intubated patients, confirm endotracheal tube (ETT) placement and monitor ventilation to avoid hyperoxia or hypoxia, as well as hypercapnia or hypocapnia.

Hemodynamic Support:

  • Prevent and treat hypotension using parenteral fluids and vasoactive medications, guided by physiologic endpoints and cardiac function.
  • Monitor for signs of recurrent shock and intervene promptly.

Glucose Management:

  • Maintain blood glucose levels below 180 mg/dL to avoid complications associated with hyperglycemia.

Seizure Management:

  • For unconscious children after ROSC, continuous electroencephalography monitoring is also recommended to detect subclinical seizures. Seizures should be monitored and treated aggressively, as they can exacerbate neurological injury.

Temperature Regulation:

  • Avoid hyperthermia (core temperature >37.5°C) using cooling measures as necessary to reduce metabolic demands and limit neuronal damage.

Summary

Pediatric CA remains a critical event with high mortality and significant morbidity. Unlike adult CA, pediatric cases are often precipitated by respiratory failure and hypoxia, highlighting the need for timely recognition and intervention. Early identification of abnormal vital signs, particularly through tools like PEWS, and a structured approach to initial assessment using the ABCDE framework are paramount in preventing CA. Furthermore, rapid and effective resuscitation, incorporating high-quality CPR, advanced airway management, and appropriate medication use, significantly improves the likelihood of survival and favorable outcomes.

Managing pediatric CA extends beyond achieving ROSC. Comprehensive post-cardiac arrest care, including targeted temperature management, optimized ventilation and oxygenation, hemodynamic support, glucose management, and seizure control, is critical to minimize secondary injuries and improve neurological recovery. Pediatric Advanced Life Support (PALS) algorithms and effective resuscitation team dynamics play essential roles in guiding care.

Ultimately, improving outcomes in pediatric CA requires a systematic approach to prevention, timely recognition, prompt intervention, and evidence-based post-resuscitation care. Continuous education, training, and adherence to updated guidelines are essential for healthcare providers to ensure the best possible outcomes for critically ill or arrested children.

Authors

Picture of Burak Çakar

Burak Çakar

Gaziantep Islahiye State Hospital, Department of Emergency Medicine, Gaziantep, Turkey

Picture of Ayça Koca

Ayça Koca

Ayça Koca is an emergency physician at Ankara University School of Medicine, Department of Emergency Medicine. She completed both her medical degree and residency at Ankara University, where she developed a deep connection to patient care and teaching. With a special interest in medical education and simulation, she is passionate about creating engaging learning experiences to support the growth and confidence of future healthcare providers.

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Reviewed and Edited By

Picture of Elif Dilek Cakal, MD, MMed

Elif Dilek Cakal, MD, MMed

Picture of Arif Alper Cevik, MD, FEMAT, FIFEM

Arif Alper Cevik, MD, FEMAT, FIFEM

Prof Cevik is an Emergency Medicine academician at United Arab Emirates University, interested in international emergency medicine, emergency medicine education, medical education, point of care ultrasound and trauma. He is the founder and director of the International Emergency Medicine Education Project – iem-student.org, chair of the International Federation for Emergency Medicine (IFEM) core curriculum and education committee and board member of the Asian Society for Emergency Medicine and Emirati Board of Emergency Medicine.

Peripheral Intravenous Line Access and Blood Sampling (2024)

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by Omar F. Al- Nahhas, Mansoor M. Husain

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Introduction

Peripheral IV Cannulation is a critical skill for healthcare providers in the Emergency Department, clinics, and the field. Knowing that it is one of the most essential procedures in the United States, where it is estimated that more than 25 million patients have peripheral intravenous (IV) catheters placed each year for vascular access for the administration of medications and fluids and the sampling of blood for analysis [1], makes it essential to master the technique, understand the subtleties of anatomy, and perform the procedure frequently to maintain this skill.

IV access plays a critical role in the emergency department as it permits the administration of medicines and fluids directly into the patient’s bloodstream, allowing prompt treatment of severe conditions such as dehydration, shock, and severe infections. The speed of treatment delivery is crucial in emergency scenarios, and peripheral IV access provides an efficient and effective way to deliver life-saving therapies. Additionally, it enables the frequent and easy sampling of blood, which is crucial for diagnosing and monitoring the patient’s condition. Therefore, healthcare providers in the emergency department must develop quick and reliable peripheral IV access skills to guarantee the best possible patient outcomes.

Indications

  • Administration of fluids: Patients who are dehydrated or unable to tolerate oral fluids may require IV fluids to maintain hydration and electrolyte balance [2].
  • Medication administration: Certain medications, such as antibiotics, chemotherapy drugs, and pain relievers, may need to be administered intravenously to achieve the desired effect.
  • Blood transfusions: Patients who have lost a significant amount of blood due to trauma or surgery may require a blood transfusion via an IV cannula.
  • Monitoring: IV access may be necessary for frequent blood draws or to monitor certain parameters, such as blood glucose levels.
  • Contrast material administration: Some imaging studies, such as CT scans, require the administration of contrast material via IV cannulas to help visualize certain structures.

Contraindications

There are no absolute contraindications. Relative contraindications include

  • Coagulopathy
  • The presence of local infection
  • Burns, or compromised skin at the intended site of insertion
  • Previous lymphatic nodal clearance, arteriovenous fistula formation, or deep venous thrombosis on the affected limb.

In such cases, clinical judgment must be used to balance the benefits and risks of proceeding with line placement at that site [2].

Equipment and Patient Preparation

Equipment

  • Gloves
  • Skin disinfectant (Povidine and Alcohol Swabs),
  • 16-18 gauge IV catheter (smaller catheters are better used in the pediatric population)
  • Tape
  • Syringe
  • 3-way stopcock
  • Tourniquet

Optional

  • Topical anesthetic, e.g., EMLA ( 2.5% lidocaine and prilocaine),
  • Transilluminator light
  • Ultrasound with a vascular probe.

Patient Preperation

To perform the procedure, obtaining consent from the patient after discussing the procedure and its associated risks and benefits is important. The preferred site for cannulation is the Cephalic vein in the forearm, followed by the Medial Brachial Vein in the Antecubital Sulcus.  The dorsum of the hand is also a common site, but this can be more painful for the patient, and often, smaller gauge cannulas are used. Always use universal precautions, such as wearing gloves, during the procedure. The selected vein should be visualized and palpated, as it will have a slight “give” compared to surrounding tissue.

The overlying skin should be disinfected, and a topical anesthetic may be applied as desired. While transillumination or ultrasound may provide additional guidance, care should be taken to avoid contamination of the clean, prepped site to be accessed.

Procedure Steps

The procedure for peripheral IV cannulation involves several steps [3]:

  1. Apply a tourniquet or blood pressure cuff inflated above the diastolic reading proximal to the intravenous site.
  2. Prepare the site with an antiseptic solution.
  3. Insert the IV catheter using a no-touch technique distal to and along the line of the vein at a 10 to 15-degree angle to the skin.
  4. Slowly advance the needle and catheter into the vein, waiting for a flash of blood to enter the catheter, which may not always occur.
  5. Slowly advance the needle an additional 1 to 2 millimeters and slide the cannula into the vein while securing the needle in place.
  6. Remove the needle while pressing on the overlying skin over the cannula proximal to the insertion site to stem the blood flow.
  7. Attach a 3-way stopcock and flush the stopcock and cannula with 5 ml of saline to prevent clotting. Assess the fluid flow through the catheter and watch for skin bulge, which may suggest fluid extravasation.
  8. Secure the catheter with tape or dressing and release the tourniquet or blood pressure cuff.
  9. Attach intravenous tubing to the 3-way stopcock, attach it to the fluid of choice, and initiate flow. Watch again for fluid extravasation. Medications may be administered through another port of the stopcock or added to the IV solution as desired.
  10. Ensure that the tourniquet is removed before administering drug or fluid infusion.
  11. If fluid extravasation occurs, remove the catheter and repeat the procedure at a more proximal site, avoiding distal attempts.
  12. These steps should be performed carefully and with appropriate attention to detail to ensure successful IV cannulation.

Blood Sampling

Blood sampling is a fundamental procedure in clinical practice for diagnostic and monitoring purposes. Various tubes are available for collecting blood samples, each designed for specific laboratory tests. For instance, the Vacutainer system offers a range of tubes with different additives to facilitate accurate test results. The choice of the tube depends on the required analyses, such as complete blood count (CBC), basic chemistry panels, coagulation studies, blood cultures, or specialized tests. Adhering to the appropriate tube selection based on the intended tests is crucial for obtaining reliable laboratory results. The amount of blood required for each tube varies depending on the specific test being conducted.

Generally, a CBC requires 2-4 mL of blood to obtain sufficient quantities of plasma or serum for cell counting and differential analysis [4]. Basic chemistry panels often necessitate larger volumes, ranging from 5-10 mL, to provide enough serum or plasma for multiple analytes, such as electrolytes, liver function tests, and renal function tests [4].On the other hand, blood culture bottles usually require 10 mL of blood to optimize the sensitivity of microbial detection [5]. Understanding the recommended blood volumes for each tube is crucial for ensuring adequate sample collection and accurate test results.

In summary, proper tube selection is essential for blood sampling to ensure accurate laboratory results. Various tubes with specific additives are available and tailored for different tests. The amount of blood needed for each tube varies depending on the type of analysis being conducted. Familiarity with the recommended blood volumes for each tube is crucial to obtaining sufficient sample quantities and optimizing diagnostic accuracy.

Complications

Despite the widespread use, IV cannulation is not without complications.

Phlebitis: This refers to vein inflammation, which can cause redness, warmth, and pain at the catheter site. The incidence of phlebitis ranges from 2% to 50% in adult patients and is related to various factors, including catheter gauge, insertion site, and duration of catheterization. [6]

Catheter-related bloodstream infections (CRBSIs): These are serious infections that can result from the colonization of the catheter by microorganisms. The incidence of CRBSIs is estimated to be 1-10% and is associated with prolonged catheterization, immunocompromised patients, and inadequate catheter site care.[7]

Infiltration and extravasation: Infiltration occurs when the fluid administered leaks into the surrounding tissue, while extravasation occurs when the medication or solution irritates the surrounding tissue, leading to tissue damage. The incidence of infiltration ranges from 4% to 38%, while extravasation occurs in less than 6% of patients. [8]

Hematoma: This is a collection of blood at the site of the catheter, which can occur due to trauma during catheter insertion or catheter displacement. Hematoma is reported in 0.5-8% of cases. [9]

Nerve injury: Nerve injury can occur due to direct trauma during catheter insertion, leading to motor and sensory deficits. The incidence of nerve injury is low, reported in less than 1% of cases. [10]

In conclusion, peripheral IV catheterization is a commonly performed procedure but not without complications. Careful attention to technique and site care can help minimize the risks of complications.

Hints and Pitfalls

To successfully perform peripheral IV cannulation, it’s important to use the correct technique and select an appropriate site with a visible vein.

  • Start by applying heat and a tourniquet to enhance blood flow, making the vein more prominent.
  • Once you have identified the vein, stabilize it and insert the cannula at an angle of 10 to 30 degrees, advancing it slowly while monitoring for proper placement.
  • Finally, secure the cannula using a transparent dressing or tape, ensuring it is not too tight.

Proper care and maintenance of peripheral intravenous (IV) lines are crucial to prevent complications and ensure patient safety. According to evidence-based guidelines, dressing care plays a vital role in IV line maintenance. Transparent semipermeable dressings are recommended by the Infusion Nurses Society (INS) as they provide a barrier against contamination and allow easy visualization of the insertion site [11]. Regular inspection of the dressing is important to identify any issues such as loosening, soiling, or moisture accumulation, and compromised dressings should be promptly replaced using sterile technique to reduce the risk of infection.

Flushing and locking peripheral IV lines are essential for maintaining patency. The INS recommends flushing with 0.9% sodium chloride (normal saline) solution before and after medication administration and at least every 8-12 hours for continuous infusions [11]. This practice helps prevent blood clot formation and ensures proper line functioning. When intermittent infusion is not expected for an extended period, the INS suggests using a saline or heparin lock to maintain line patency [11].

Vigilant monitoring and assessment of the peripheral IV site are critical to detect any signs of infection or complications. According to the Centers for Disease Control and Prevention (CDC), routine site inspection should be performed at least daily, paying close attention to redness, swelling, warmth, tenderness, or drainage [12]. Timely reporting and appropriate intervention in case of any abnormalities are crucial to prevent complications like phlebitis or infiltration.

Patient education is an essential aspect of peripheral IV line care. Educating patients and their caregivers about proper hand hygiene, signs of infection or complications, and when to seek medical assistance is vital. Patients should receive clear instructions to promptly report any pain, tenderness, or changes at the IV site.

It is important to note that specific institutional protocols may vary, and adherence to local guidelines is essential. These recommendations are based on current evidence and best practices in peripheral IV line care, aiming to promote patient safety and achieve optimal outcomes.

There are some pitfalls to avoid. Failure to use proper technique or choosing an inappropriate site can increase the risk of infection and complications such as infiltration, extravasation, or phlebitis. Applying too much heat or pressure with the tourniquet can cause burns or damage to the veins. Failure to stabilize the vein or inserting the cannula at the wrong angle can make cannulation more difficult or cause complications. Advancing the cannula too quickly or over-tightening the dressing can cause pain or discomfort, restrict blood flow, or damage the vein.

In time-critical cases with known difficult peripheral access or where multiple attempts at peripheral line placement have already failed, an ultrasound-guided technique may be necessary, or the clinician may consider using alternative routes of drug administration (such as oral, intramuscular, intraosseous, or central venous access).

Special Patient Groups

Certain populations, including pediatric, geriatric, and pregnant patients, require special considerations during peripheral IV catheterization.

Pediatrics

Pediatric patients have unique anatomical and physiological differences that affect the success of IV catheterization. The smaller size of their veins and thinner skin can make it challenging to locate and access suitable sites for catheter insertion [13]. 

Additionally, children have a higher risk of experiencing pain, discomfort, and anxiety during the procedure, which can lead to complications such as vasovagal syncope and catheter dislodgement. Therefore, healthcare providers need to use appropriate-sized catheters and consider non-pharmacological interventions, such as distraction techniques and topical anesthetics, to minimize the pain and discomfort associated with the procedure [13].

Geriatrics

Geriatric patients also require special consideration during peripheral IV catheterization. As individuals age, their veins become less elastic and more fragile, making it challenging to cannulate veins and increasing the risk of complications such as hematoma, infiltration, and extravasation. Furthermore, geriatric patients often have multiple comorbidities and take multiple medications, which can increase the risk of adverse reactions and interactions with IV medications. Therefore, healthcare providers must assess the patient’s venous status and consider alternative routes of medication administration when appropriate [14].

Pregnant Patients

Pregnant patients pose unique challenges during peripheral IV catheterization due to the physiological changes that occur during pregnancy. Increased blood volume, decreased venous compliance, and increased peripheral resistance make locating and accessing suitable veins for catheter insertion difficult. Additionally, certain medications and fluids can affect the mother and fetus, requiring careful consideration of the medication’s safety and potential risks. Therefore, healthcare providers can use ultrasound guidance and consider the patient’s gestational age, medical history, and current medications when selecting the site and medication for IV catheterization [15].

In summary, peripheral IV catheterization requires special considerations in pediatric, geriatric, and pregnant patients. Healthcare providers should assess the patient’s anatomical and physiological status and select appropriate-sized catheters. They should also consider non-pharmacological interventions to reduce pain and discomfort and carefully select the site and medication for IV catheterization to minimize the risk of complications.

Authors

Picture of Omar F. Al- Nahhas

Omar F. Al- Nahhas

Dr. Omar Al-Nahhas is a Senior Emergency Medicine Resident at STMC, Al-Ain, UAE, and an MSc Candidate in Medical Education at the University of Warwick. He is an Adjunct Clinical and Simulation Tutor at Ajman University and a certified BLS and ACLS Instructor. With publications in emergency medicine, his interests include Trauma, Sports Medicine, Critical care and Advanced Emergency Medicine, emphasizing education, research, and resuscitation practices.

Picture of Mansoor M. Husain

Mansoor M. Husain

Consultant Emergency Medicine, Tawam Hospital – Alain

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References

  1. Chopra V, Anand S, Hickner A, Buist M, Rogers MA, Saint S, Flanders SA. “Risk of venous thromboembolism associated with peripherally inserted central catheters: a systematic review and meta-analysis.” Lancet. 2013 Jul 27;382(9889):311-25. doi: 10.1016/S0140-6736(13)60592-9. Epub 2013 May 30. PMID: 23726390.
  2. Beecham GB, Tackling G. Peripheral Line Placement. [Updated 2022 Jul 25]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2023 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK539795/
  3. Keith A. “Intravenous (IV) Line Access” (n.d.). International Emergency Medicine Education Project, Available athttps://iem-student.org/intravenous-iv-line-access/.
  4. Clinical and Laboratory Standards Institute (CLSI). (2017). Procedures for the Collection of Diagnostic Blood Specimens by Venipuncture; Approved Standard—Eighth Edition. CLSI Document GP41-A8. CLSI.
  5. Clinical and Laboratory Standards Institute (CLSI). (2020). Principles and Procedures for Blood Cultures; Approved Guideline—Third Edition. CLSI Document M47-A3. CLSI.
  6. Helm RE, Klausner JD, Klemperer JD, et al. Accepted but unacceptable: peripheral IV catheter failure. J Infus Nurs. 2015;38(3):189-203.
  7. Blot SI, Depuydt P, Annemans L, et al. Clinical and economic outcomes in critically ill patients with nosocomial catheter-related bloodstream infections. Clin Infect Dis. 2005;41(11):1591-1598.
  8. Dougherty L, Lister S. Infusion Nursing: An Evidence-Based Approach. Elsevier Health Sciences; 2014.
  9. Feleke Y, Mekonnen N, Assefa A. Magnitude and associated factors of intravenous catheter-related hematoma in the adult emergency department of Tikur Anbessa Specialized Hospital, Addis Ababa, Ethiopia. BMC Emerg Med. 2018;18(1):10.
  10. Wallis MC, McGrail M, Webster J, et al. Risk factors for peripheral intravenous catheter failure: a multivariate analysis of data from a randomized controlled trial. Infect Control Hosp Epidemiol. 2014;35(1):63-68.
  11. Infusion Nurses Society. (2021). Infusion therapy standards of practice. Journal of Infusion Nursing, 44(1S), S1-S224.
  12. Centers for Disease Control and Prevention. (2021). Guidelines for the Prevention of Intravascular Catheter-Related Infections. Retrieved from https://www.cdc.gov/infectioncontrol/guidelines/bsi/index.html
  13. Naik VM, Mantha SSP, Rayani BK. Vascular access in children. Indian J Anaesth. 2019 Sep;63(9):737-745. doi: 10.4103/ija.IJA_489_19. PMID: 31571687; PMCID: PMC6761776.
  14. Gabriel, J. (2017). Understanding the challenges to vascular access in an ageing population. British Journal of Nursing, 26(14), S15–S23. doi:10.12968/bjon.2017.26.14.s
  15. Tan PC, Mackeen A, Khong SY, Omar SZ, Noor Azmi MA. Peripheral Intravenous Catheterisation in Obstetric Patients in the Hand or Forearm Vein: A Randomised Trial. Sci Rep. 2016 Mar 18;6:23223. doi: 10.1038/srep23223. PMID: 26987593; PMCID: PMC4796788.

Reviewed and Edited By

Picture of Arif Alper Cevik, MD, FEMAT, FIFEM

Arif Alper Cevik, MD, FEMAT, FIFEM

Prof Cevik is an Emergency Medicine academician at United Arab Emirates University, interested in international emergency medicine, emergency medicine education, medical education, point of care ultrasound and trauma. He is the founder and director of the International Emergency Medicine Education Project – iem-student.org, chair of the International Federation for Emergency Medicine (IFEM) core curriculum and education committee and board member of the Asian Society for Emergency Medicine and Emirati Board of Emergency Medicine.

Basics of Bleeding Control (2024)

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by Tasnim Ahmed & Abdulla Alhmoudi

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Introduction

The primary objective in the resuscitation of traumatic hemorrhage is to achieve effective hemostasis and maintain hemodynamic stability. The severity of bleeding depends on the depth of the wound and the type of injured vessel. The approach to bleeding control should be tailored to the type and size of the bleeding vessel and the specific anatomical regions involved. Delayed or ineffective haemorrhage management can complicate the healing process and, in severe cases, lead to fatality. Extremity haemorrhage has historically contributed significantly to high mortality rates from casualties during wars [1]. Therefore, the prompt implementation of appropriate haemostatic techniques is a crucial aspect of efficient trauma management. This critical task is typically initiated by the prehospital team and followed by more advanced, invasive techniques provided by the trauma team in a controlled hospital setting

Types of Wounds

Wound is an impairment to the structural integrity of biological tissues, including the skin, mucous membranes, and organ tissues. This disruption in tissue integrity may arise from a diverse range of causes, including traumatic injuries, pathological processes, or surgical interventions. Metric parameters such as size (length), depth, shape, and whether they are open or closed are used to describe wounds.

The subsequent descriptors represent the terminology utilized for the classification of wounds:

Contusions

Contusions result from perpendicular blunt force to the skin, usually through a layer of clothes. Rupture of subcutaneous capillaries can occur, resulting in the formation of a hematoma (Figure 1). The recommended management for this type of wound consists of analgesics and following the “RICE” protocol (Rest, Ice, Compression, and Elevation) [2].

Figure 1 - Contusion

Abrasion

Abrasion is the scraping or scratching of the surface layers of skin (epidermis) when subjected to oblique forces (Figure 2). Proper wound care involves cleansing the wound, applying a sterile bandage, administering analgesics, ensuring tetanus protection, and implementing the RICE protocol [2].

Figure 2 - Abrasion

Incision

Incision is defined as a cut that features straight edges along the margins of the wound. It can be caused by sharp objects like scalpels, knives, sharp metal pieces, or glass (Figure 3). Tissue loss is uncommon, and the wound margins can be easily aligned for closure with medical glue or sutures [1,2,3].

Figure 3 - Incision

Lacerations

Characterized irregular or jagged edges, appearing torn rather than neat incisions [1,3]. They can have an irregular or linear direction and may branch out (Figure 4). Objects with broken or serrated edges or blunt impact on tissue overlying bone typically cause lacerations. Treatment approaches for lacerations are similar to those for incision wounds. However, the appropriate subspecialty should manage deep, complex lacerations or those involving sensitive areas like the face, joints, or tendons.

Figure 4 - Laceration

Avulsion

Avulsion involves a full-thickness laceration-type wound, which usually creates a flap of tissue (Figure 5) [1,3]. Mechanical accidents involving fingers (degloving injuries) can cause avulsions. More severe cases may include exposure of internal organs. Avulsions are challenging to repair and should never be considered minor injuries.

Figure 5 - Avulsion

Amputation

Amputations differ from avulsions in that they involve the complete loss of a limb, whereas avulsions result in the loss of just a flap of skin (Figure 6). It can occur at any point along an extremity and is usually accompanied by significant arterial bleeding. Despite the seriousness of this injury, a properly cooled and transported amputated limb may sometimes be surgically reattached in a hospital setting.

Figure 6 - Amputation

Puncture and Penetrating Wounds

Puncture and penetrating wounds result from the penetration of a sharp object into the tissue without lateral movement from the point of entry (Figure 7). Puncture wounds can be deceptive, as they may appear small on the surface but extend deeply, potentially damaging the neurovascular structure or internal organs and causing significant internal bleeding or secondary injuries. 

Figure 7 - Puncture wound with soft tissue infection

Stab wounds from knives or sharp objects, as well as bullet wounds, are examples of penetrating injuries [1,2,3]. Occasionally, the penetrating object may remain logged to the injury and should never be removed without careful assessment by the trauma team, as it might act as mechanical hemostatic and result in further bleeding once removed. 

Site of Injury

Injuries can also be classified into three types, depending on the injured site of the body; each entails a different approach to management. Extremity injuries refer to damage inflicted on the blood vessels of the arms or legs. Junctional injuries, on the other hand, involve vascular damage occurring at the junction where the extremities meet the torso, such as the hip, axilla, or base of the neck. Torso injuries often involve non-compressible truncal hemorrhage that occurs anywhere on the torso and involves large blood vessels.

Vascular Injury

Injury to any blood vessel type can result in external bleeding. The specific type of vascular injury can be identified based on the characteristics of bleeding observed [1,2,4].

The following are the distinct types of vascular injuries and their corresponding patterns of bleeding:

Arterial Bleeding

Arterial bleeding typically occurs as a consequence of deep penetrating injuries or amputations. It is distinguished by the forceful ejection of bright red blood from the wound synchronized with each heartbeat [2]. Complete laceration of the artery may trigger spontaneous constriction, which helps to control bleeding. However, if only the artery wall is damaged without complete dissection, it can lead to persistent bleeding.

Indicators of arterial injury are classified into hard signs and soft signs [2]. Identifying hard signs indicates an immediate need for arterial exploration and surgical intervention. To aid in the recollection of these hard signs, the mnemonic “The Broken PIPE” can be employed (Box 1). Conversely, soft signs indicate the necessity for additional investigations such as ankle-brachial index measurement, Duplex Doppler ultrasound, or CT angiography, as determined by clinical assessment. The soft signs can be represented by the mnemonic “NON-Deadly HemorrHage” (Box 2).

Venous Bleeding

Venous Bleeding is characterized by a slower flow of dark red blood out of the wound [2]. However, caution is still recommended in venous bleeding, as it can contribute to significant and rapid bleeding if left untreated [4].

Capillary Bleeding

Capillary Bleeding usually results from damage to subcutaneous capillaries. It is characterized by slow, intermittent bleeding in the form of dots or small oozing [2,4].

Indications of Bleeding Control Techniques

Achieving hemodynamic stability necessitates the effective control of all life- or limb-threatening bleeding. While in most cases of traumatic and non-traumatic resuscitation, emphasis is placed on managing the airway and ensuring proper breathing, in situations of exsanguinating bleeding, prioritizing massive hemorrhage control surpasses the immediate focus on airway and breathing management [1]. The choice of hemostatic technique should be based on the depth and specific location of the injury, as outlined in detail in the “Bleeding Control Techniques” section below.

Contraindications of Bleeding Control Techniques

There are no absolute contraindications to any specific hemostatic method [1]. However, bleeding injuries should not distract the physician from managing concurrent immediate life-threatening conditions. Additionally, immediate wound closure is not recommended in wounds older than 8 hours. Instead, these types of wounds should be cleaned thoroughly, covered with sterile dressing, and closed after 3-5 days if there are no signs of infection. This is referred to as “delayed primary closure” [2,3].

Preparation

Similar to all medical procedures, thorough preparation is essential to ensure efficient hemostasis. This preparation encompasses the healthcare team, equipment, medications, the patient, and the wound.

Team Preparation

The healthcare providers involved in the procedure should possess comprehensive knowledge of indications, contraindications, techniques, and potential complications. The team should wear appropriate personal protective equipment, including face masks, face shields, surgical gowns, gloves, and shoe covers as necessary [3]. This protective gear is crucial to safeguard against blood splashes and potential contact with body fluids, particularly in trauma settings where the patient’s health status may be unknown.

Equipment Preparation

The equipment and medications used for hemostasis must be meticulously prepared and checked for the expiry date and functionality. The required equipment is listed under the corresponding techniques in the “Bleeding Control Techniques” section below.

Patient Preparation

A detailed explanation of the procedure should be provided to the patient, and informed consent should be obtained if applicable. Additionally, securing intravenous access and collecting a blood sample for type and cross-matching and coagulation profile are imperative. Administering analgesics and local anesthetics before procedural maneuvers helps to effectively minimize patient discomfort and disruptive movements.

Wound Preparation

A thorough assessment of the wound should be conducted. Distal movement and neurovascular function should be assessed prior to any manipulation. Contaminated wounds require proper irrigation to remove foreign bodies, followed by sterilization of the surrounding skin using antiseptic solution such as povidone iodine or chlorhexidine. However, wound preparation should not delay definitive hemostatic measures [1,3]. 

Bleeding Control Techniques

Direct Pressure

The initial step in controlling bleeding involves applying direct pressure to the bleeding wound. This facilitates the formation of a platelet plug and the initiation of the physiologic coagulation cascade, which is typically achievable within 10 to 15 minutes of proper pressure application [1]. 

Equipment

  • Sterile gauze pad size 4×4
  • Compression bandage
  • Splint\brace

Technique

Ensuring the proper replacement of skin flaps is essential, followed by placing multiple 4×4 sterile gauzes, ideally low adherent type, with equal pressure applied. The wound can be wrapped with a compression bandage if it is in the head or extremities. Following the application of a compression bandage to the extremities, distal mobility, sensation, and perfusion should be checked. Limbs should be placed in a brace to minimize movement and keep it elevated. In body junctions, the wound can alternatively be packed with gauze or hemostatic agents along with topical pressure application [1,2,4].

Precautions

It is important to avoid removing soaked gauze, as this can function as a foreign clot; instead, a new gauze should be applied on top of the existing ones [4]. Compression bandages should be avoided in thoracic wounds, as they can constrict breathing.

Pressure on Arteries

When the source of bleeding cannot be identified, applying proximal pressure can help control the bleeding by reducing blood flow to the injured artery [1].  This is only feasible with extremity wounds and should not be applied to the carotid artery, as this can precipitate ischemic brain insult or vagal stimulation, resulting in bradycardia [4].

Precautions

The time of application is limited to 10 minutes due to the risk of tissue necrosis distal to the pressure point.

Tourniquet

The indication to use tourniquets is severe extremity bleeding that is not controlled by direct pressure application. The concept is constricting arterial flow to the injured area. It is an extremely painful procedure, and proper analgesia should be ensured before applying a tourniquet if time allows.

Equipment

  • Proper size tourniquet
  • Alternative: Blood pressure cuff

Technique

Remove any clothing obstructing the tourniquet application site, ensuring it is directly applied to the skin and remains visible. Position the tourniquet approximately 2-3 inches above the wound, avoiding joints (Figure 8). Tighten the tourniquet until the bleeding stops and the pulse distal to the tourniquet is no longer palpable. Note the time of placement on the tourniquet tag or consider using an indelible marker to write it on patient’s skin. [4,5].

Figure 8 - Tourniquet application

If bleeding is not controlled and the distal pulse is still present after applying the first tourniquet, apply a second one just above its location [4]. Increasing the width of the second tourniquet is more effective in controlling bleeding and reducing complications than excessively tightening the initial one. Administer analgesia as needed after the tourniquet is applied.

An alternative to the tourniquet is applying a blood pressure cuff proximal to the wound. The cuff is then inflated 20-30 mm Hg above systolic blood pressure or over 250 mm Hg, and the tubing is clamped with a hemostat [2]. There are many ways to improvise a tourniquet using non-stretchable clothing and a windlass rod like a pen; however, a commercially designed tourniquet is preferable and not likely to loosen easily with patient movement. 

To safely remove the tourniquet, apply a pressure dressing directly onto the wound. Then, gradually release the tourniquet while carefully monitoring for any signs of bleeding. If bleeding is successfully controlled, keep the tourniquet loosely secured in case of potential re-bleeding. If bleeding recurs, reapply firm pressure by tightening the tourniquet [5].

Precautions

The maximum duration for tourniquet application is 120 minutes [2]. Prolonged tourniquet application can lead to complications such as nerve injury, tissue necrosis, compartment syndrome, and rhabdomyolysis. However, if the extremity is amputated or if the tourniquet has been applied for more than 6 hours, it should not be loosened as permanent muscle damage occurs after 6 hours and might require amputation.1 Moreover, potential reperfusion injury may occur after 60 minutes of tourniquet use, leading to inflammation-induced damage in local areas and systemic effects on vital organs caused by inflammatory mediators [5].

Topical Hemostatic Agents

Another alternative or adjunct to tourniquet use is topical hemostatic agents. These agents create a platform for platelet deposition and facilitate hemostasis [6]. Examples include [1] oxidized cellulose (e.g., Surgicel), dry gelatin (e.g., Gelfoam, Surgifoam), or cyanoacrylate.

Equipment

  • Hemostatic agent (e.g., Combat Gauze, Celox Gauze, or ChitoGauze)
  • Pressure dressing

Technique

The hemostatic gauze is applied with direct pressure for at least 3 minutes. After the field dries, the wound can be sutured, or pressure dressing can be applied. It is important to note that a dry field is required to apply the cyanoacrylate type. Pressure or tourniquet should be used before its application. An alternative to hemostatic gauze is topical thrombin. It can be used directly or diluted with saline and sprayed onto the wound. A concentration of 100 units/mL is effective. In severe bleeding, a concentration of 1000 to 2000 units/mL can be used [1].

Precautions

Potential complications associated with hemostatic agents include excessive granulation tissue and fibrosis with absorbable gelatin agents or foreign body reaction with cellulose [1,7].

Balloon Catheter

Balloon catheters can be used as an improvised tamponade technique to temporarily control severe bleeding from deep injuries, when other conventional methods fail [1,8].

Equipment

  • Fogarty catheters, Foley catheters, or Sengstaken-Blakemore tubes.
  • 10 cc syringe

Technique

The tube is blindly inserted into the wound, then the ballon is inflated to halt bleeding from deep vascular injuries [1].

Suture Ligation

Suture ligation is used for controlling large bleeding vessels. An effective ligation technique requires careful examination and knowledge of the vascular anatomy to trace and identify the sources of bleeding. A retracted artery can be a potential source of delayed bleeding. Therefore, once an injured vessel is identified, the opposite end should also be traced and ligated [1]. 

Equipment

  • Blood pressure cuff
  • Absorbable suture (e.g., Vicryl, Monocryl, and PDS).
  • Haemostat
  • Needle holder
  • Scissors

Technique

A blood pressure cuff is placed proximally and inflated until the bleeding stops to create a clear field. With gradual deflation of the cuff, large bleeding vessels will start to be visible. Ligation is then completed with suturing in the following steps: [1]

  1. Using a haemostat pinch the free end of the bleeding vessel.
  2. Wrap a proper-sized suture around the vessel.
  3. Tie the suture at the base of the vessel.
  4. Release the haemostat carefully (Figure 9).

if the vessel can not be seen, a figure 8 suture can be applied (Figure 10) [1,3]. 

Figure 9 - Vessel ligation technique. (1) Grasp the cut end of the bleeding vessel with a haemostat. (2) Pass an appropriately sized suture around the vessel. (3) Tie and secure the suture around the base of the bleeding vessel. (4) Gently release the haemostat from the blood vessel. (Freeman C, Reichman EF. Hemorrhage Control. In: Emergency Medicine Procedures. 6th ed. Elsevier; 2020:112-1. "Control of the Bleeding Vessel that is Visualized." Adapted and redrawn by Tasnim Ahmed, MD).
Figure 10. Figure 8 stich. A. Needle directions, B.Tie. (Freeman C, Reichman EF. Hemorrhage Control. In: Emergency Medicine Procedures. 6th ed. Elsevier; 2020:112-2. "Control of a Bleeding Vessel Deep or Embedded in Tissue." Adapted and redrawn by Tasnim Ahmed, MD).

Cauterization

Cauterization is cost effective and simple haemostatic technique for small vessels measuring less than 2 mm in diameter. Electrical cauterization  involves using electrical current to heat an electrode, which then is used to thermally burn the vessel wall and seal it with charred tissue [1,10]. 

Chemical cauterization can be achieved using silver nitrate (AgNO3). This involves applying the agent to the vessel wall using an applicator, typically a long and small wooden stick tipped with the silver nitrate. Silver nitrate reacts with proteins in the tissue, forming an insoluble deposit that blocks the blood flow. It is only effective when applied to a dry tissue or minimal oozing [1]. 

Equipment

  • Blood pressure cuff
  • Silver nitrate or electric cautery

Technique

Position a blood pressure cuff proximally and gradually inflate it until bleeding stops, to achieve a clear field. Then gently release the pressure, until the smaller bleeding vessels become visible. Use the electrocautery to burn the end of the bleeding vessel or rub the silver nitrate against it to achieve an artificial clot [1].

Vasoconstrictors

In normal conditions, small vessels spontaneously stop bleeding. However, if bleeding persists, local vasoconstrictors mixed with local anaesthetics can be applied. Local anesthetic solutions containing epinephrine, such as lidocaine and bupivacaine, are readily available in the Emergency Department.

Equipment

  • 10 cc syringe
  • Epinephrine 1:1000
  • Saline-soaked gauze

Technique

Prepare the diluted epinephrine in a 10 cc syringe. Aspirate prior to injection to ensure that the solution is not injected into a blood vessel. Inject 1 to 2 mL of the solution around the bleeding vessel. Apply direct pressure with saline soaked gauze over the wound. Alternatively, spray the wound with the diluted solution. [1,3]

Precautions

It’s important to avoid using epinephrine or other vasoconstrictors in end-arterial areas like fingers, toes, ears, nose, or penis, to avoid organ ischemia.

Complications

Complications arise when the above-listed techniques are either overused or applied inappropriately. For detailed information regarding the particular complications associated with each technique, please refer to the corresponding technique’s “Precautions” section.  

Special Patient Groups

Obtaining hemostasis might be challenging in patients with coagulopathy. Therefore, it is important to remain vigilant and promptly assess the platelet count and plasma coagulation profile (PT/PTT/INR) in patients experiencing external bleeding. The early administration of tranexamic acid, blood products, and cryoprecipitate can aid in achieving hemostasis.

Authors

Picture of Tasnim Ahmed

Tasnim Ahmed

Emergency Medicine Residency graduate from Zayed Military Hospital, Abu Dhabi, UAE. Deputy Editor-in-Chief of the Emirates Society of Emergency Medicine (ESEM) newsletter. Senior Board Member and Website Manager of the Emirates Collaboration of Residents in Emergency Medicine (ECREM). Awarded Resident of the Year twice, at ESEM23 and Menatox23. Passionate about medical education, with a focus on blending art and technology into innovative teaching strategies.

Picture of Abdulla Alhmoudi

Abdulla Alhmoudi

Dr Abdulla Alhmoudi is a Consultant Emergency Medicine, serving at Zayed Military Hospital and Sheikh Shakhbout Medical City - Abu Dhabi. He pursued his residency training in Emergency Medicine at George Washington University in Washington DC and further enhanced his expertise with a Fellowship in Extreme Environmental Medicine. Dr Alhmoudi's passion for medical education is evident in his professional pursuits. He currently holds the position of Associate Program Director at ZMH EM program and is a lecturer at Khalifa University College of Medicine and Health Sciences. Beyond medical education, he maintains a keen interest in military medicine and wilderness medicine.

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References

  1. Chapter 112. Hemorrhage Control. In: Reichman EF. eds. Emergency Medicine Procedures, 2e. McGraw Hill; 2013. Accessed May 22, 2023. https://accessemergencymedicine.mhmedical.com/content.aspx?bookid=683&sectionid=45343754
  2. Spehonja A, Prosen G. Basics of Bleeding Control. In: Cevik AA, ed. International Emergency Medicine Education Project. iEM Education Project; 2018:598-601.
  3. Lammers RL, Smith ZE. Principles of wound management. In: Roberts JR, Hedges JR, eds. Roberts & Hedges’ Clinical Procedures in Emergency Medicine. 6th ed. Philadelphia, PA: Elsevier; 2014:611-634.
  4. Department of the Navy. Bleeding. Brooksidepress.org. 2001. Accessed May 22, 2023. https://www.brooksidepress.org/Products/OperationalMedicine/DATA/operationalmed/Manuals/Standard1stAid/chapter3.html.
  5. Lee C, Porter KM, Hodgetts TJ. Tourniquet use in the civilian prehospital setting. Emergency Medicine Journal. 2007;24(8):584-587. doi:10.1136/emj.2007.046359
  6. Sileshi B, Achneck HE, Lawson JH. Management of surgical hemostasis: topical agents [published correction appears in Vascular. 2009 May-Jun;17(3):181]. Vascular. 2008;16 Suppl 1:S22-S28.
  7. Levy JH. Hemostatic agents and their safety. J Cardiothorac Vasc Anesth. 1999;13(4 Suppl 1):6-37.
  8. Feliciano DV, Burch JM, Mattox KL, Bitondo CG, Fields G. Balloon catheter tamponade in cardiovascular wounds. Am J Surg. 1990;160(6):583-587. doi:10.1016/s0002-9610(05)80750-0
  9. Rudge WB, Rudge BC, Rudge CJ. A useful technique for the control of bleeding following peripheral vascular injury. Ann R Coll Surg Engl. 2010;92(1):77-78. doi:10.1308/rcsann.2010.92.1.77
  10. Kamat AA, Kramer P, Soisson AP. Superiority of electrocautery over the suture method for achieving cervical cone bed hemostasis. Obstet Gynecol. 2003;102(4):726-730. doi:10.1016/s0029-7844(03)00622-7

Reviewed and Edited By

Picture of Arif Alper Cevik, MD, FEMAT, FIFEM

Arif Alper Cevik, MD, FEMAT, FIFEM

Prof Cevik is an Emergency Medicine academician at United Arab Emirates University, interested in international emergency medicine, emergency medicine education, medical education, point of care ultrasound and trauma. He is the founder and director of the International Emergency Medicine Education Project – iem-student.org, chair of the International Federation for Emergency Medicine (IFEM) core curriculum and education committee and board member of the Asian Society for Emergency Medicine and Emirati Board of Emergency Medicine.

Gastroenteritis and Dehydration In Children (2024)

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by Neha Hudlikar & Abdulla Alhmoudi 

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You have a new patient!

14-month-old Zoey is brought to A&E by her mother with complaints of vomiting and diarrhea for one day. She has had six episodes of vomiting and eight episodes of loose stools since last night. She has also not had a wet diaper for almost 12 hours now. In triage, her vitals are HR 165 b/min, RR 45 br/min, Temperature 38.5 C, SpO2 97% CR 3 seconds. The nurse in triage notes that she has a glazed look. She is otherwise fit and well, with no past medical history. Zoey’s weight – 10 kg.

What will be your approach for this patient?

a-photo-of-a-baby (image produced by using ideogram2.0)

What do you need to know?

Importance

Acute gastroenteritis is one of the most common reasons for visits to pediatric emergency departments [1]. The World Health Organization (WHO) defines diarrhea as the passage of three or more liquid stools per day, or a more frequent passage than what is normal for the individual. When diarrhea occurs alongside vomiting, it is referred to as acute gastroenteritis (AGE).

Diarrhea can be categorized into three clinical types based on the presence or absence of blood and the timing of symptoms:

1. Acute watery diarrhea – lasts from hours to several days, but less than 14 days.
2. Acute bloody diarrhea – also known as dysentery, lasts less than 14 days.
3. Persistent diarrhea – lasts longer than 14 days.

Infectious gastroenteritis can be caused by various pathogens, including viruses, bacteria, and parasites. Rotavirus is the most common causative agent worldwide, responsible for 37% of diarrhea-related deaths in children under five years of age.

Epidemiology

Gastroenteritis is the second leading cause of death in children below the age of 5 and a leading cause of malnutrition in this age group. Globally, there are approximately 1.7 billion cases of childhood diarrheal diseases yearly, and the burden is substantial [2]. There is a direct impact of admission costs on the hospital budget and direct and indirect societal costs when children are admitted to hospitals.

In low-income countries, children under three years old, on average, have three episodes of diarrhea every year. This puts them at risk of malnutrition and, in turn, makes them vulnerable to further episodes of infectious diarrhea.

Pathophysiology

The loss of water and electrolytes via stools, vomit, sweat, and urine without adequate replacement leads to dehydration, a serious complication of gastroenteritis. Physiologic factors that predispose children to serious complications from dehydration include limited stores of fat and glycogen, relatively larger extracellular fluid compartments, and a limited ability to conserve water through their kidneys compared to adults.

Bicarbonate loss in stools, decreased tissue perfusion leading to anaerobic metabolism and lactic acid production, ketosis due to starvation, and decreased excretion of hydrogen ions due to poor renal perfusion are some of the mechanisms contributing to metabolic acidosis in pediatric dehydration due to acute gastroenteritis.

The exact pathophysiology depends on the causative agent. Infectious agents cause diarrhea via adherence, mucosal invasion, enterotoxin, and cytotoxin production.S. aureus and Bacillus cereus produce heat-stable enterotoxins in the food, which once consumed, lead to rapid onset of symptoms and are usually self-limiting. C. Perfingens, Enterotoxigenic E.coli produce enterotoxins in the small intestine leading to watery diarrhea. Other pathogens like enterohemorrhagic E. Coli (EHEC), Salmonella, Shigella, and Campylobacter jejuni produce toxins that directly invade the bowel leading to inflammatory diarrhea. Viruses often destroy the villus surface of the intestinal mucosa, and parasites often adhere to the mucosa.

Medical History

A focused and detailed history is essential to narrowing our differential diagnoses and guiding management. The history should include the timing, frequency, and severity of symptoms. We should also ask about any contact with someone with similar symptoms, known or suspected outbreaks in school or nursery, and recent travel.

All patients with acute gastroenteritis are at risk of dehydration, and the initial evaluation should include questions to assess its severity. The child’s oral intake, amount of urine passed, mental status (lethargy/irritability), etc., should be asked for in the initial evaluation. 

It is also important to ask for associated symptoms such as fever, abdominal pain, blood in the stools, and rash. Children with inflammatory diarrhea can develop serious illnesses like hemolytic uremic syndrome (HUS) with renal involvement. 

Other important questions in history include the child’s vaccination status, recent hospitalization/antibiotic use, and whether the child has any underlying chronic medical conditions/immunosuppression.

Physical Examination

Examining the child should be systematic, looking for the severity of dehydration and differentiating gastroenteritis from other causes of vomiting and diarrhea in children.

General examination should include the child’s appearance, alertness, lethargy, irritability, and weight. Vital signs should be assessed relative to the age. Physicians should look for explicit signs of dehydration, such as dry mucous membranes, sunken eyes, depressed fontanelle, and the presence/absence of tears. The cardiovascular exam should include heart rate, quality of pulses, and central and peripheral capillary refill times. Deep, acidotic breathing suggests severe dehydration. An abdominal examination assesses tenderness, bowel sounds, guarding, and rebound. Flank tenderness increases the likelihood of pyelonephritis. Examine the skin to check skin turgor, peripheral temperature, and other signs such as jaundice/rash.

Abnormal skin turgor, prolonged capillary refill time, and abnormal respiratory pattern are the three most useful examination findings in children with more than 5% dehydration [3]. It is important to note that these signs can be subtle, and determining the severity of dehydration accurately is challenging for physicians.

Alternative Diagnoses

Dehydration most commonly results from acute gastroenteritis in children. However, other diagnoses should be considered based on physical examination and history. Children with fever who are very ill-looking should have sepsis as one of the differential diagnoses. Other diagnoses to consider are urinary tract infection, appendicitis, hemolytic uremic syndrome, intussusception, and diabetic ketoacidosis. Symptoms immediately after ingestion should prompt physicians to consider ingestion of a foreign body or toxic substance. 

Vomiting and diarrhea are two important components that ED practitioners need a careful evaluation to rule in or out various diseases.

When evaluating vomiting in children, it is essential to consider a wide range of differential diagnoses spanning several systems. Central nervous system causes include space-occupying lesions, hydrocephalus, and infections. Cardiac-related vomiting may be attributed to congestive heart failure from various etiologies. Gastrointestinal conditions such as intussusception, midgut volvulus, pyloric stenosis, appendicitis, and esophageal or hepatic disorders are significant considerations. Renal issues like urinary tract infections, pyelonephritis, renal insufficiency, and renal tubular acidosis can also manifest as vomiting. Furthermore, metabolic and endocrine abnormalities, including diabetic ketoacidosis, Addisonian crisis, congenital adrenal hyperplasia, and inborn errors of metabolism, are key causes. Infectious conditions such as sepsis, pneumonia, otitis media, streptococcal pharyngitis, and gastroenteritis must also be included in the diagnostic workup.

Diarrhea in children can arise from diverse causes. Gastrointestinal disorders such as intussusception, Hirschsprung’s disease with toxic megacolon, inflammatory bowel disease, and appendicitis are prominent. Renal conditions, including urinary tract infections and pyelonephritis, can also lead to diarrhea. Infectious etiologies like sepsis, pneumonia, gastroenteritis, and pseudomembranous colitis are frequent contributors. Other causes include drug effects or overdose, hemolytic uremic syndrome, and congenital secretory diarrhea.

Understanding these potential causes is essential for accurate diagnosis and effective management.

Acing Diagnostic Testing

The workup should be guided by history and physical examination to determine the level of dehydration. In most cases, it is a self-limiting disease, and the principal goal of testing in ED should be to identify and correct fluid, electrolyte, and acid-base deficits. 

Most children with mild to moderate disease require no diagnostic testing. Children requiring IV hydration should have blood gas, serum electrolytes, bicarbonate, urea, and creatinine levels tested. It is common for young children to have hypoglycemia, and checking serum glucose levels is important. In children presenting with fever or mucous/blood in their stools, consider testing for fecal leucocytes to support a diagnosis of invasive diarrhea. A positive test should be followed by a stool culture, and it is important to note that a negative test does not rule out invasive disease.

Consider additional testing, such as blood and urine cultures, chest X-rays, and lumbar puncture, in immunosuppressed patients, infants less than 2 months old, or children with suspicion of bacteremia or localized invasive disease. 

Risk Stratification

The Gorelick scale and The Clinical Dehydration Score (CDS) are two of the most widely used scoring systems to predict the presence and severity of dehydration in the pediatric population. It is important to note that neither can definitively rule in or out dehydration in children and infants. Physicians should continue to use a structured approach to patients presenting with acute gastroenteritis and use these scores to aid clinical decision-making [4,5,6].

Clinical Dehydration Scale

 

0

1

2

 

0: No dehydration (<3%)

1-4: Some dehydration (≥3%- <6%)

5-8: Moderate dehydration (≥6%)

General appearance

Normal

Thirsty, restless or lethargic but irritable when touched

Drowsy, limp, or comatose

Eyes

Normal

Slightly sunken

Very sunken

Mucous membranes

Moist

“Sticky”

Dry

Tears

Present

Decreased

Absent

 

Gorelick Scale for Dehydration

characteristic

no or minimal dehydration

moderate to severe dehydration

general appearance

alert

restless, lethargic, unconscious

capillary refill

normal

prolonged or minimal

tears

present

absent

mucous membrane

moist

dry, very dry

eyes

normal

sunken; deeply sunken

breathing

present

deep; deep and rapid

quality of pulses

normal

thready; weak or impalpable

skin elasticity

instant recoil

recoil slowly; recoil > 2 s

heart rate

normal

tachycardia

urine output

normal

reduced; not passed in many hours

Evaluating dehydration with Gorelick scale [6];

4-Point Scale (Italics):

  • 4 points: Presence of 2 or more clinical signs correlating with ≥5% body weight loss from baseline.
  • 4 points: Presence of 3 or more clinical signs correlating with ≥10% body weight loss from baseline.

10-Point Scale (Based on All Signs and Symptoms):

  • ≥3 clinical signs: Associated with ≥5% body weight loss from baseline.
  • ≥7 clinical signs: Associated with ≥10% body weight loss from baseline

Some groups are at higher risk of developing complications from acute gastroenteritis. These include premature infants, very low birth weight infants, and infants below the age of 3 months. Children who are malnourished, immunosuppressed, and with chronic underlying medical conditions are also at higher risk of developing complications.

Indications for inpatient management of children presenting with acute diarrhea have been proposed, and the Table below summarizes these recommendations.

Indications for Inpatient Management of Children with Acute Diarrhoea

  • Difficulties in administrating oral rehydration therapy (patient refusal, intractable vomiting)
  • History of premature birth, chronic medical conditions, or concurrent illness, very young age
  • Parental/caregiver concern about continuing ORT at home/unable to provide adequate care
  • Persistent vomiting, high output diarrhoea, persistent dehydration
  • Uncertainty of diagnosis warranting further observation
  • Progressive symptoms or unusual irritability/drowsiness
  • Lack of easy access to hospital care if needing to return

Adapted from King CK, Glass R, Bresee JS, Duggan C; Centers for Disease Control and Prevention. Managing acute gastroenteritis among children: oral rehydration, maintenance, and nutritional therapy. MMWR Recomm Rep. 2003;52(RR-16):1-16.

Management

Management in the Emergency Department should initially focus on correcting dehydration. Oral rehydration solution (ORS) is recommended for all children with mild to moderate dehydration.

To calculate the volume of oral replacement therapy (ORT), the first step is to estimate the degree of dehydration based on history and physical examination findings (see Table below). The desired volume of ORS is then calculated based on the degree of dehydration (30 to 50 mL/kg for mild and 60 to 80 mL/kg for moderate dehydration). 25% of the calculated volume of ORS is given every hour for the first four hours and ongoing losses can be replaced at 10 mL/kg for each stool and 2 mL/kg for each emesis. The patient needs reassessment at the end of the first few hours and those with no clinical deterioration may have a 2 to 4-hour trial with ORT. If the child is unable to keep up with ongoing losses and if volume replacement is not adequate at the end of 8 hours, IV rehydration is recommended. Ondansetron is a selective 5-hydroxytryptamine type 3 receptor antagonist, a useful adjunct in treating AGE. It acts on peripheral and central chemoreceptors to alleviate nausea. It has been shown to decrease vomiting, improve oral intake, and reduce the need for intravenous fluid resuscitation and hospital admissions [7].

Assessment of Degree of Dehydration

Mild dehydration (3%-5%)

Moderate dehydration (5%-10%)

Severe dehydration (> 10%)

Mental status

Alert

Irritable

Lethargy

Heart rate

Normal

Increased

Increased

Quality of pulses

Normal

Normal to decreased

Decreased to thready

Mucous membranes

Wet

Slightly dry

Dry

Capillary refill

< 2 seconds

> 2 seconds

> 2 seconds

Blood pressure

Normal

Normal

Normal to decreased

Respirations

Normal

Tacypnea

Tachypnea, deep

Fontanelle

Normal

Sunken

Sunken

Eyes

Normal

Slightly sunken, decreased tears

Sunken, cries without tears

Urine output

Normal to decreased

Decreased

Oliguric or anuric

Skin turgor

Normal

Slightly reduced

Reduced

Children with severe dehydration, signs of shock, failed attempts with oral rehydration therapy, intractable vomiting, hypoglycemia, or electrolyte derangements require intravenous fluid resuscitation, which is often initiated as a 20 mL/kg bolus of 0.9% of sodium chloride in ED. These patients need frequent re-evaluation to review their response to IV hydration. Improvements in mental status, tachycardia, capillary refill time, and urine production are some signs that signal a good response to intravenous resuscitation. After initial resuscitation, patients will need an evaluation of their maintenance fluid needs, which could be either intravenous fluid therapy or ORT, depending on the patient’s clinical status. Maintenance fluids are calculated based on the child’s weight using the 4-2-1 Holliday-Segar Rule.

Holliday-Segar Rule for Maintenance Fluid Calculation

Body Weight

mL/kg/hr

mL/kg/day

First 10 kg

4

100

Second 10 kg

2

50

Each additional kg

1

20

Children who require multiple fluid boluses without signs of improvement should be investigated for other serious conditions such as adrenal insufficiency, cardiogenic or septic shock, etc. It is important to note that rapid correction of serum sodium levels can lead to osmotic demyelination syndrome in hyponatremia and cerebral edema in hypernatremia.

In children with hypoglycemia, glucose can be replaced as per the “rule of 50,” where the percent dextrose multiplied by the number of mL per kilogram equals 50. Neonates often get 10% dextrose solution at 5mL/kg, children between 1 month to 8 years of age (or 25 kg weight) can be given 2mL/kg of 25% dextrose. 50% of dextrose at 1mL/kg can be used safely in older children. The higher tonicity of 25% and 50% dextrose solutions poses a risk of tissue necrosis if extravasation occurs during peripheral IV infusion.
 
Antibiotics are not indicated in viral gastroenteritis and most cases of uncomplicated bacterial gastroenteritis. Considerations can be made for very young infants, immunocompromised, and those with chronic underlying medical conditions. The WHO recommends zinc supplementation for children under 5 years suffering from AGE in developing countries [8]. Studies showing the efficacy of probiotics are inconclusive and further research is needed to establish the safety and efficacy of probiotics in children with AGE [9].

When To Admit This Patient

Most cases of AGE are self-limiting and can be managed on an outpatient basis after a brief period of observation in the ED. Parents and caregivers should be given appropriate discharge instructions emphasizing hygiene and hand-washing techniques to prevent the further spread of the illness. Breastfeeding/routine diet should be continued at home, and supplemental electrolyte solutions may be recommended. Parents and caregivers should be educated to recognize the signs of dehydration and advised to bring the child back to the ED for these. Children with intractable vomiting, severe dehydration, failure to maintain oral hydration, electrolyte derangements, deteriorating clinical status, and those at high risk for complications (very low birth weight infants, < 3 months old, immunosuppressed, and children with chronic medical problems) should be admitted to hospital.

Revisiting Your Patient

History-taking reveals that Zoey has not had much to drink or eat in the past 12 hours, and there has been an outbreak of gastroenteritis in the nursery that she attends. There has been no blood in the stools, and Mum says that Zoey has been very sleepy for the last few hours. Her vaccinations are up to date, and she has no other medical history of note.

On examination, she is irritable when you approach her, and your systematic examination reveals the following:
CNS – Irritable, no signs of meningism, anterior fontanelle closed
HEENT – Dry mucous membranes, slightly sunken eyeballs
Respiratory – Mild tachypnea, bilateral air entry with clear breath sounds
CVS – Central capillary refill 3 seconds, tachycardia, BP 88/50
Abdomen – Soft, lax and non-tender. Bowel sounds ++, no mass palpable
Skin – Slightly reduced skin turgor, no rash

Next steps?

Your examination reveals no red flags of meningitis/sepsis or surgical abdomen. Given the recent outbreak of gastroenteritis in her nursery, you make a provisional diagnosis of acute gastroenteritis for Zoey. Your clinical assessment estimates the degree of dehydration to be moderate (5-10%), and you calculate her fluid depletion to be between 600 to 800 mL (60 to 80 mL/kg). You start the patient on oral rehydration therapy aiming for at least 200 mL to be given slowly over the next hour. You guide the mother in letting the staff know if Zoey vomits or has another episode of diarrhea while in the Emergency Department.

Investigations?

You ask for a random blood sugar to rule out hypoglycemia and a urine dipstick to rule out urinary tract infection.

Review
After an hour, Zoey tolerated 250 mL of oral rehydration solution and had one episode of vomiting but no diarrhea. Her blood sugar was 4 mmol/l. She has perked up significantly and is more alert than before. Her vital signs show improvement, and you decide to give her Ondansetron and continue the ORT.

After two hours, Zoey has tolerated around 400 mL of ORS and is more alert and interactive now. Her vitals are normal, and she has not had any further episodes of diarrhea or vomiting. She has also passed some urine, which has been tested and found to be negative for infection.

Mum was advised to continue oral hydration at home as well as the slow introduction of a regular diet and to come back to ED if Zoey could not tolerate orally, had intractable vomiting, any blood in her stools, high-grade fever, or change from her baseline mental status. Zoey was discharged from the ED and would follow up with her primary physician in the community.

Authors

Picture of Neha Hudlikar

Neha Hudlikar

Emergency Department, Zayed Military Hospital, Abu Dhabi

Picture of Abdulla Alhmoudi

Abdulla Alhmoudi

Dr Abdulla Alhmoudi is a Consultant Emergency Medicine, serving at Zayed Military Hospital and Sheikh Shakhbout Medical City - Abu Dhabi. He pursued his residency training in Emergency Medicine at George Washington University in Washington DC and further enhanced his expertise with a Fellowship in Extreme Environmental Medicine. Dr Alhmoudi's passion for medical education is evident in his professional pursuits. He currently holds the position of Associate Program Director at ZMH EM program and is a lecturer at Khalifa University College of Medicine and Health Sciences. Beyond medical education, he maintains a keen interest in military medicine and wilderness medicine.

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References

  1. McDermott KW, Stocks C, Freeman WJ. Overview of Pediatric Emergency Department Visits, 2015. In: Healthcare Cost and Utilization Project (HCUP) Statistical Briefs. Rockville (MD): Agency for Healthcare Research and Quality (US); August 7, 2018.
  2. Hartman RM, Cohen AL, Antoni S, et al. Risk Factors for Mortality Among Children Younger Than Age 5 Years With Severe Diarrhea in Low- and Middle-income Countries: Findings From the World Health Organization-coordinated Global Rotavirus and Pediatric Diarrhea Surveillance Networks [published correction appears in Clin Infect Dis. 2023 Jan 6;76(1):183]. Clin Infect Dis. 2023;76(3):e1047-e1053. doi:10.1093/cid/ciac561
  3. Steiner MJ, DeWalt DA, Byerley JS. Is this child dehydrated?. JAMA. 2004;291(22):2746-2754. doi:10.1001/jama.291.22.2746
  4. Falszewska A, Szajewska H, Dziechciarz P. Diagnostic accuracy of three clinical dehydration scales: a systematic review. Arch Dis Child. 2018;103(4):383-388. doi:10.1136/archdischild-2017-313762
  5. Freedman SB, Vandermeer B, Milne A, Hartling L; Pediatric Emergency Research Canada Gastroenteritis Study Group.
  6. Pringle K, Shah SP, Umulisa I, et al. Comparing the accuracy of the three popular clinical dehydration scales in children with diarrhea. Int J Emerg Med. 2011;4:58. Published 2011 Sep 9. doi:10.1186/1865-1380-4-58
  7. Tomasik E, Ziółkowska E, Kołodziej M, Szajewska H. Systematic review with meta-analysis: ondansetron for vomiting in children with acute gastroenteritis. Aliment Pharmacol Ther. 2016;44(5):438-446. doi:10.1111/apt.13728Diagnosing clinically significant dehydration in children with acute gastroenteritis using noninvasive methods: a meta-analysis. J Pediatr. 2015;166(4):908-16.e166. doi:10.1016/j.jpeds.2014.12.029
  8. Goldman RD. Zinc supplementation for acute gastroenteritis. Can Fam Physician. 2013;59(4):363-364.
  9. Cameron D, Hock QS, Kadim M, et al. Probiotics for gastrointestinal disorders: Proposed recommendations for children of the Asia-Pacific region. World J Gastroenterol. 2017;23(45):7952-7964. doi:10.3748/wjg.v23.i45.7952

Additional Resources

King CK, Glass R, Bresee JS, Duggan C; Centers for Disease Control and Prevention. Managing acute gastroenteritis among children: oral rehydration, maintenance, and nutritional therapy. MMWR Recomm Rep. 2003;52(RR-16):1-16.

Reviewed and Edited By

Picture of Arif Alper Cevik, MD, FEMAT, FIFEM

Arif Alper Cevik, MD, FEMAT, FIFEM

Prof Cevik is an Emergency Medicine academician at United Arab Emirates University, interested in international emergency medicine, emergency medicine education, medical education, point of care ultrasound and trauma. He is the founder and director of the International Emergency Medicine Education Project – iem-student.org, chair of the International Federation for Emergency Medicine (IFEM) core curriculum and education committee and board member of the Asian Society for Emergency Medicine and Emirati Board of Emergency Medicine.

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Cardiac Monitoring (2024)

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by Stacey Chamberlain

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Definitions and Overview

Cardiac monitoring in the emergency setting is continuous monitoring of a patient’s cardiac activity in order to identify conditions that may require emergent intervention. These conditions include certain arrhythmias, ischemia and infarction, and abnormal findings that could signal impending decompensation. This chapter focuses specifically on cardiac monitoring or electrocardiography; additional methods of continuous hemodynamic monitoring in the emergency department (ED) include pulse oximetry, end-tidal CO2 monitoring, central venous pressure monitoring, and continuous arterial blood pressure monitoring. Of note, telemetry is the ability to do cardiac monitoring from a remote location; in practice, this is often a centralized system that might be located at a nursing station where multiple patients can be monitored remotely.

Cardiac monitoring differs from a 12-lead electrocardiogram in that it is done continuously over a period of time rather than capturing one moment in time in a static image. The benefit of this is that it captures transient arrhythmias and ectopic beats or monitors for changes over time. A disadvantage of cardiac monitoring is that typically, only 2 leads are displayed instead of a full 12 leads, giving a less comprehensive view of the heart and limiting its utility for looking for anatomic patterns. For example, on the 12-lead EKG, ED practitioners usually group the inferior, anterior, and lateral leads when looking for ischemic or infarct patterns. These may be less evident on a monitor with only two leads. Additionally, the static EKG allows the ED physician to carefully study it for subtle findings, for example, to make measurements of intervals, whereas in real-time monitoring, this is very difficult. In practice, both modalities are commonly used in conjunction for many ED patients.

The American Heart Association (AHA) published a consensus document in 2004 establishing practice standards for electrocardiographic monitoring in hospital settings, which was updated in 2017 [1,2]. These comprehensive documents outline the indications for cardiac monitoring, the specific skills required of the practitioner for cardiac monitoring, and specific ECG abnormalities that the practitioner should recognize. The 2017 update addressed the overuse of arrhythmia monitoring among certain populations, appropriate use of ischemia and QT-internal monitoring among select populations, alarm management, and documentation in electronic health records [2].

Cardiac monitoring is essential for those patients who are at risk for an acute, life-threatening arrhythmia and can also be used to evaluate for developing ischemia, response to therapy, and as a diagnostic tool. The AHA guidelines divide indications for cardiac monitoring in the inpatient setting into four classes based on varying degrees (level A, B, C) of evidence. Cardiac monitoring is considered indicated in patients in Class I. In Class IIa, it “is reasonable to perform” cardiac monitoring, whereas in Class IIb, it “may be considered.” For Class III, cardiac monitoring is not indicated as there is no benefit or there may actually be harm. Newer guidelines tailor the recommendations based on specific patient populations and whether the cardiac monitoring is for arrhythmia or continuous ST-segment ischemic monitoring [2]. Specific patient populations that are considered include patients with:

  1. Chest pain or coronary artery disease.
  2. Major cardiac interventions such as open heart surgery.
  3. Arrhythmias.
  4. Syncope of suspected cardiac origin.
  5. After electrophysiology procedures/ablations.
  6. After pacemaker or ICD implantation procedures.
  7. Pre-existing rhythm devices.
  8. Other cardiac conditions (acute decompensated heart failure or infective endocarditis).
  9. Non-cardiac conditions (e.g., post-conscious sedation or post-non-cardiac surgery).
  10. Specific medical conditions (e.g., stroke, imbalance of potassium or magnesium, drug overdose, or hemodialysis).
  11. DNR/DNI status.

Table 1 lists Class I-III recommendations. The AHA Scientific Statement provides a more comprehensive and detailed list.

Table 1 – Select Indications for Cardiac Monitoring

Class I Indications

Early phase ACS or after MI

 

After open-heart surgery or mechanical circulatory support

 

Atrial tachyarrhythmias

 

Symptomatic sinus bradycardia

 

2nd or 3rd degree AV block (exception as noted below for asymptomatic Wenckebach)

 

Congenital or genetic arrhythmic syndrome (e.g. WPW, Brugada, LQTS)

 

After stroke

 

With moderate to severe imbalance of potassium or magnesium

 

After drug overdose

Class IIa and IIb Indications

Non-sustained VT

 

Asymptomatic, significant bradycardia with negative chronotropic medications initiated

 

After non-cardiac major thoracic surgery

 

Chronic hemodialysis patients without other indications (e.g. hyperkalemia, arrhythmia)

Class III Indications

After non-urgent PCI without complications or after routine diagnostic coronary angiography

 

Patients with chronic atrial fibrillation, sinus bradycardia, or asymptomatic Wenckebach who are hemodynamically stable and admitted for other indications

 

Asymptomatic post-operative patients after non-cardiac surgery

 

DNR/DNI patients when the data will not be acted on and comfort-focused care is the goal

Ischemia Monitoring

Continuous ST-Segment Ischemia Monitoring was highlighted in the 2017 AHA guidelines as a specific indication for cardiac monitoring for patients most at risk for ischemia. Older monitors may not have this capability, but more modern monitors are programmed with automated ischemia monitoring that identifies abnormal ST-segment elevation or depression; manufacturers do not automatically enable this capability, and it may be turned on or off. To reduce unnecessary alarms, it is recommended (IIa level) to enable this function only in high-risk patients in the early phase of ACS and to individualize which lead should be prioritized based on the coronary artery suspected to be affected by an ischemic process. High-risk patients would include those being evaluated for vasospastic angina, those presenting with MI, post-MI patients without revascularization or with residual ischemic lesions, and newly diagnosed patients with a high-risk lesion such as a left main blockage.

QTc Monitoring

QTc monitoring aims to assess the safety of QT-prolonging medications and avoid Torsade de Pointes (TdP). Most hospitals do not have fully automated continuous QTc monitoring, so QTc monitoring and measurements may need to be performed manually or semi-automated with digital calipers. Regardless of the method, in general, recommendations for QTc monitoring are for patients with specific risk factors for TdP who are started on anti-arrhythmic drugs with a known risk for TdP (e.g., dofetilide, sotalol, procainamide, quinidine, and others), patients with a history of prolonged QTc started on non-anti-arrhythmic drugs with risk for TdP, those undergoing targeted temperature management, specific electrolyte derangements, and select drug overdoses. As with ischemic monitoring, QTc monitoring is not universally recommended for all patients, so consulting the 2017 guidelines for select patient scenarios is best.

Rhythm Interpretation

One of the most critical skills of an ED physician is in interpreting both static EKGs and interpreting arrhythmias on a cardiac monitor. A skilled practitioner must be able to diagnose common arrhythmias and be well-versed in the management of acute arrhythmias, recognizing which arrhythmias necessitate immediate action and which are less worrisome. Table 2 from the 2004 AHA guidelines lists the specific arrhythmias that the ED physician must be able to recognize. How and whether to treat an arrhythmia depends on many factors. The AHA has established algorithms for specific rhythms, including ventricular fibrillation (v-fib)/pulseless ventricular tachycardia (v-tach) and pulseless electrical activity (PEA)/asystole, as well as for non-specific rhythm categories such as bradycardia and tachycardia [3]. Additionally, they have published algorithms for clinical scenarios, including cardiac arrest, acute coronary syndrome, and suspected stroke.

The first step in the assessment of any rhythm is a clinical assessment of the patient. The premier issue of concern is if the patient is perfusing vital organs. A quick survey of the patient assessing mental status and pulses is essential to determining management. The management of a patient with v-tach will be substantially different if the patient is unresponsive and pulseless versus if the patient is awake with good pulses. As another example, the physician can quickly distinguish artifact from v-fib on the cardiac monitor by assessing the patient, as v-fib is not a perfusing rhythm.

The initial assessment of tachyarrhythmias (heart rate > 100) is to determine if the rhythm is “narrow-complex” (i.e., a QRS duration < 0.12s) or “wide-complex” (i.e., a QRS duration of 0.12s or greater). A narrow complex rhythm is considered a supraventricular rhythm (originating above the ventricles). Supraventricular tachycardia is a generic term encompassing any narrow-complex tachycardias originating above the AV node. Colloquially, when many practitioners refer to “SVT,” however, they are referring to a specific subcategory of supraventricular tachycardia called AV nodal re-entrant tachycardia (AVNRT). Wide complex tachycardias either originate in the ventricles or could originate in the atria and have an associated bundle branch block. Different criteria have been developed to help the practitioner distinguish between ventricular tachycardia and an SVT “with aberrancy” (i.e., aberrant conduction either due to an accessory path such as in Wolff-Parkinson-White or with a bundle branch block), the most well known of which are the Brugada criteria [4,5]. Practically speaking, many ED practitioners will assume the more dangerous and potentially unstable rhythm (v-tach) until proven otherwise; of course, the clinical picture and the patient’s vital signs are of utmost importance in determining the management of these patients. An excellent summary of this issue with rhythm strip examples is provided on the FOAM site “Life in the Fast Lane” [6].

Table 2 – Specific Arrythmias (adapted from AHA Scientific Statement [1])

Normal rhythms

 

 

Normal sinus rhythm

 

Sinus bradycardia

 

Sinus arrhythmia

 

Sinus tachycardia

Intraventricular conduction defects

 

 

Right and left bundle-branch block

 

Aberrant ventricular conduction

Bradyarrhythmias

 

 

Inappropriate sinus bradycardia

 

Sinus node pause or arrest

 

Non-conducted atrial premature beats

 

Junctional rhythm

AV blocks

 

 

1st degree

 

2nd degree Mobitz I (Wenckebach) or Mobitz II

 

3rd degree (complete heart block)

Asystole

 

Pulseless electrical activity (PEA)

 

Tachyarrhythmias

 

 

Supraventricular

Paroxysmal supraventricular tachycardia (AV nodal reentrant, AV reentrant)

Atrial fibrillation

Atrial flutter

Multifocal atrial tachycardia

Junctional ectopic tachycardia

Accelerated ventricular rhythm

Ventricular

Monomorphic and polymorphic ventricular tachycardia

Torsades de pointes

Ventricular fibrillation

Premature complexes

 

 

Supraventricular (atrial, junctional)

 

Ventricular

Pacemaker electrocardiography

 

 

Failure to sense

 

Failure to capture

 

Failure to pace

ECG abnormalities of acute myocardial ischemia

 

 

ST-segment elevation, depression

 

T-wave inversion

Muscle or other artifacts simulating arrhythmias

 

While each rhythm has distinctive management, it is worth noting for the novice learner that only v-fib and pulseless v-tach warrant asynchronized mechanical defibrillation (i.e. “shocking” the patient). Many students are stunned upon observing an asystolic cardiac arrest code to learn that shocking a “flatline” (i.e., asystolic) patient is an inappropriate treatment perpetuated by fictitious TV shows and movies. For unstable patients with arrhythmias but still have palpable pulses, synchronized cardioversion may be used.

Regarding medications, for certain rhythms and clinical scenarios, only vasopressor types of medications are used (e.g., epinephrine for asystole). For other rhythms and scenarios, antiarrhythmic medications are used (e.g., amiodarone for v-tach). Atrioventricular (AV) nodal blocking agents are often necessary for supraventricular tachyarrhythmias. One author suggests using a five “As” approach to treating emergency arrhythmias, keeping in mind the medications adenosine, amiodarone, adrenaline (epinephrine), atropine, and ajmaline [7]. Ajmaline is an antiarrhythmic that is not commonly used in English-speaking countries where procainamide is more common as an alternative to amiodarone for unstable v-tach.

Additional interventions may include pacemaker placement for symptomatic heart blocks. In many cases, the ED practitioner must also determine the underlying precipitant of the arrhythmia and tailor treatment to that cause. The emergency physician must familiarize himself with each rhythm and its unique management in any given clinical scenario.

At the end of this chapter, some good internet resources for the ED practitioner to practice interpreting EKGs and cardiac rhythms are provided.

Case Example

A 44-year-old male patient with a history of hypertension and end-stage renal disease on hemodialysis presents with shortness of breath after missing dialysis for 6 days. He reports gradual onset shortness of breath associated with orthopnea and increased lower extremity edema. He denies chest pain or palpitations. He does not have any cough or fever. On physical exam, he is in no distress, afebrile with a heart rate of 60, respiratory rate of 20, blood pressure of 140/78 mmHg, and oxygen saturation of 98% on room air. He has a regular rate and rhythm without murmurs and has crackles bilaterally to the inferior 1/3 of the lung bases and 1+ pitting edema of the bilateral lower extremities.

You decide to get an EKG, which shows the following:

Figure 1 (EKG from http://www.lifeinthefastlane.com)

You send a blood chemistry test, place the patient on a cardiac monitor, and one hour later note the following on the monitor:

Figure 2 - (EKG from liftl.com)

What are the indications for cardiac monitoring in this patient? What EKG abnormalities do you see? What does the rhythm strip show? What is the treatment?

Case Discussion

The ED practitioner should recognize potentially life-threatening conditions that a patient who has missed hemodialysis is at risk for are fluid overload (leading to pulmonary edema) and hyperkalemia. This patient could be considered to meet the Class I monitoring criteria for “needing intensive care” and possibly with “pulmonary edema”; however, even if the patient had no symptoms, the patient is indeed at risk for an acute life-threatening arrhythmia that would necessitate cardiac monitoring.

The EKG demonstrates peaked T waves indicative of acute hyperkalemia. Given the clinical picture of missed dialysis and the peaked Ts on the EKG, the ED physician should immediately initiate treatment for acute hyperkalemia without waiting for a confirmatory blood test (unless immediate point-of-care tests are available). If the patient’s hyperkalemia progressed, the patient could develop QRS widening with the morphology as shown on the rhythm strip called a “sine wave.” This dangerous finding could precipitously deteriorate into a life-threatening arrhythmia such as pulseless v-tach with cardiac arrest and should prompt immediate action. It is important to note that hyperkalemia can manifest in a variety of different EKG findings and does not always follow a consistent pattern from peaked Ts to QRS widening to sine waves; therefore, the patient should be treated at the first indication of any hyperkalemia-related EKG changes.

Conclusions

Cardiac monitoring is an important tool to monitor patients at risk for acute arrhythmias (including those at risk specifically for TdP) and acute or worsening cardiac ischemia. It can be helpful to immediately identify patients with life-threatening arrhythmias who need immediate intervention, to assess the response to medications for arrhythmias, and to help exclude arrhythmias as a likely etiology of a patient’s symptoms (e.g., a patient with syncope) [9]. Given the limited resources and the lack of benefits for many patients, the purpose and duration of cardiac monitoring should be carefully considered. Overuse can not only waste resources but can also contribute to alarm hazards, including “alarm fatigue,” where clinicians are barraged by so many false or nonactionable alarm signals that they become desensitized and do not respond to real events. Therefore, appropriate use and staff education are critical to maximizing the benefits of cardiac monitoring.

Author

Picture of Stacey Chamberlain

Stacey Chamberlain

Dr. Stacey Chamberlain is a board certified emergency physician who is a Professor in the Department of Emergency Medicine at the University of Illinois at Chicago (UIC). She also serves as the Director of the Global Emergency Medicine Fellowship Program and the Co-Director of the Social Emergency Medicine Fellowship Program. In addition to her work in Emergency Medicine, she is the Director of Academic Programs at the UIC Center for Global Health. In this role, she oversees the Global Medicine (GMED) Program for UIC medical students and the graduate global health certificate programs. Dr. Chamberlain has done clinical, educational, public-health, disaster-response, and emergency medicine development work, including working with several globally-focused NGOs, spanning five continents. Her global health work focuses on capacity building in emergency care in Uganda.

Listen to the chapter

2018 version of this topic – https://iem-student.org/cardiac-monitoring/

References

  1. Drew BJ, Califf RM, Funk M, Kaufman ES, Krucoff MW, et al. AHA Scientific Statement:  Practice Standards for Electrocardiographic Monitoring in Hospital Settings. Circulation. 2004; 110: 2721-2746. doi: 10.1161/01.CIR.0000145144.56673.59
  2. Sandau KE, Funk M, Auerbach A, Barsness GW, Blum K, Cvach M, Lampert R, May JL, McDaniel GM, Perez MV, Sendelbach S, Sommargren CE, Wang PJ; American Heart Association Council on Cardiovascular and Stroke Nursing; Council on Clinical Cardiology; and Council on Cardiovascular Disease in the Young. Update to Practice Standards for Electrocardiographic Monitoring in Hospital Settings: A Scientific Statement From the American Heart Association. Circulation. 2017 Nov 7;136(19):e273-e344. doi: 10.1161/CIR.0000000000000527. Epub 2017 Oct 3. PMID: 28974521.
  3. ACLS Training Center. Algorithms for Advanced Cardiac Life Support 2015. Dec 2, 2015.  Accessed at: https://www.acls.net/aclsalg.htm, Dec 10, 2015.
  4. Wellens HJJ. Ventricular tachycardia: diagnosis of broad QRS complex tachycardia. Heart2001;86:579-585 doi:10.1136/heart.86.5.579.
  5. Brugada P, Brugada J, Mont L, Smeets J, Andries EW. A new approach to the differential diagnosis of a regular tachycardia with a wide QRS complex. Circulation. 1991; 83: 1649-1659. doi: 10.1161/01.CIR.83.5.1649
  6. Burns E. VT versus SVT with aberrancy. Life in the Fast Lane. Accessed at: http://lifeinthefastlane.com/ecg-library/basics/vt_vs_svt/, Dec 10, 2015.
  7. Trappe H-J. Concept of the five ‘A’s for treating emergency arrhythmias. J Emerg Trauma Shock. 2010 Apr-Jun; 3(2): 129–136. doi:  10.4103/0974-2700.62111
  8. Ramzy M. Duration of Electrocardiographic Monitoring of Emergency Department Patients with Syncope. REBEL EM blog; June 13, 2019; Available at: https://rebelem.com/duration-of-electrocardiographic-monitoring-of-emergency-department-patients-with-syncope/.

Additional Online Resources

Reviewed and Edited By

Picture of Arif Alper Cevik, MD, FEMAT, FIFEM

Arif Alper Cevik, MD, FEMAT, FIFEM

Prof Cevik is an Emergency Medicine academician at United Arab Emirates University, interested in international emergency medicine, emergency medicine education, medical education, point of care ultrasound and trauma. He is the founder and director of the International Emergency Medicine Education Project – iem-student.org, vice-chair of the International Federation for Emergency Medicine (IFEM) core curriculum and education committee and board member of the Asian Society for Emergency Medicine and Emirati Board of Emergency Medicine.

Tachyarrhythmias (2024)

~ iEM Education Project Team ~ Leave a comment

by Keith Sai Kit Leung, Rafaqat Hussain & Abraham Ka Cheung Wai 

Authors
Listen

You have a new patient!

A 28-year-old female patient presented with 3 weeks history of palpitations. She started with a new-onset shortness of breath and dizziness this morning, which prompted her to attend ED. The patient also complains of recent unintentional weight loss, restlessness, insomnia, passing loose stool more frequently, menstrual disturbances, and some degree of chest pain. No other significant medical history was noted. On physical examination, she looks well-perfused, with bilateral equal air entry and normal vesicular breath sounds throughout, heart sound I+II with no added sound. Vital signs monitoring showed a temperature of 38.1°C, heart rate of 142 bpm, respiratory rate of 21, blood pressure of 155/98, peripheral CRT of 3s, and SpO2 96% on air. ECG is shown below:

(Source: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8496558/)

What do you need to know?

Tachyarrhythmia is an abnormal heart rate over 100 bpm. It can be classified by site of origin (sinus, supraventricular, ventricular), in relation to QRS complexes (narrow or board-complex), or regularity.

Importance

Tachycardia is an extremely common finding in patients presenting to the emergency department; it involves a wide range of differential diagnoses, from normal variants to physiological responses to life-threatening conditions like shock and cardiac arrest. Studies have shown that patients with tachycardia have an increased risk of post-discharge mortality [1, 2], with higher rates of future re-visit to ED [3].

Epidemiology and Pathophysiology

Sinus tachycardias usually occur as part of a normal physiological response (e.g., exercise, pregnancy) or a compensatory pathological response to secondary underlying conditions (e.g., pulmonary embolism, hyperthyroidism, anemia, infection). It is important to note that sinus tachycardia can be abnormal, secondary to cardiac dysautonomia. These conditions are postural orthostatic tachycardia syndrome or inappropriate sinus tachycardia.

(Reused from Jones, S. A. (2009). ECG Notes: Interpretation and Management Guide. F.A. Davis Company.)

Supraventricular tachycardias is an umbrella term that includes a number of arrhythmias that arise above the bundle of His, i.e., the sinoatrial (SA) node, atria, and atrioventricular (AV) node; these are typically narrow complex tachycardia except WPW syndrome. The most prevalent types of SVTs, in descending order, are atrial fibrillation, atrial flutter, atrioventricular nodal re-entrant tachycardia (AVNRT), atrioventricular re-entrant tachycardia (AVRT), with atrial tachycardia (AT) and junctional tachycardia being the least common types [4, 5]. Three arrhythmogenic mechanisms have been proposed: Re-entry, enhanced automaticity, or triggered activity [6].

Starting with atrial fibrillation (AF) and atrial flutter (AFL), the latest data from the Global Burden of Disease Study 2019 showed that there are 59.7 million affected individuals worldwide [7], with a male predominance in the older population. Common causes of AF include PIRATES [Mnemonic for Pulmonary embolism, Ischaemic heart disease/Idiopathic, Rheumatic valvular disorder, Anaemia/Alcohol, Thyroid (hyperthyroidism), Electrolytes imbalance/Elevated BP (hypertension), Sepsis/Sick sinus syndrome]. The arrhythmogenic mechanism of AF is by increased automaticity, leading to ectopic focal activities and the creation of micro re-entrant circuits in the atrial muscles. Without organized contractility, blood pools in the atria, predisposing to thrombus formation and increasing stroke risk.

(Reused from Jones, S. A. (2009). ECG Notes: Interpretation and Management Guide. F.A. Davis Company.)

Atrial flutter is less common than AF, but they both share similar aetiologies and may coexist. The difference between both is that AF presents with an irregularly irregular heartbeat, while AFL presents with a regularly irregular heartbeat, as a macro re-entrant circuit exists in the atrium, producing a rapid regular atrial rate at 300 bpm. Depending on the conduction ratio, affected patients have a fixed ventricular rate at 150 bpm (2:1), 100 bpm (3:1), or 75 bpm (4:1).

(Reused from Jones, S. A. (2009). ECG Notes: Interpretation and Management Guide. F.A. Davis Company.)

Atrioventricular nodal re-entrant tachycardia (AVNRT) has a prevalence of 2.25 cases per 1000 people in the general population, with a female/male ratio of 2:1 among all age groups [8]. It is the most common cause of paroxysmal SVT and occurs in about 50% of cases. Hence, it is often used synonymously with the term SVT. AVNRT is usually idiopathic, i.e., patients have structurally normal hearts. In AVNRT, re-entry is the main arrhythmogenic mechanism. Naturally, the AVN has dual pathways with different conduction velocities (a fast and slow pathway). Usually, conduction passes via the fast pathway, which blocks incoming current from the slow pathway, while in SVT, the slow pathway becomes the dominant anterograde conduction pathway, uses the fast pathway for retrograde conduction, and creates a re-entrant loop. 90% of AVNRT is slow-fast type [9].

(Reused from Jones, S. A. (2009). ECG Notes: Interpretation and Management Guide. F.A. Davis Company.)

Atrioventricular re-entrant (or reciprocating) tachycardia (AVRT) is another form of paroxysmal SVT, accounting for 30% of cases. It is caused by an anatomical re-entrant circuit with the normal AV conduction system and an AV accessory tract. The most commonly known accessory pathway is called Bundle of Kent, causing Wolff-Parkinson-White (WPW) pre-excitation syndrome; hence, WPW and AVRT are often used interchangeably. It has been estimated to affect 1-3 persons per thousand people. [10]

(Reused from Jones, S. A. (2009). ECG Notes: Interpretation and Management Guide. F.A. Davis Company.)

Atrial tachycardia (AT) accounts for the remaining 10-20% of cases, as opposed to other subtypes; it is usually caused by increased atrial automaticity independent from the AV conduction system or accessory pathways. Other causes include sinoatrial scarring, digoxin toxicity, or conditions that cause atrial dilation (COPD, CHF). Note that there are 2 types of AT, focal and multifocal AT; the former is caused by one ectopic arrhythmogenic focus and later with multiple arrhythmogenic foci within the atria. The firing rate of the ectopic focus is faster than that of the SA node, which overrides its activity. [11]

(Reused from Jones, S. A. (2009). ECG Notes: Interpretation and Management Guide. F.A. Davis Company.)
(Reused from Jones, S. A. (2009). ECG Notes: Interpretation and Management Guide. F.A. Davis Company.)
(Reused from Srinivasan C, Balaji S. Neonatal supraventricular tachycardia. Indian Pacing Electrophysiol J. 2019;19(6):222-231. DOI:10.1016/j.ipej.2019.09.004) – Open Access (https://www.sciencedirect.com/science/article/pii/S0972629219301159)

Junctional tachycardia occurs when there is increased automaticity in the AV node and decreased automaticity in the SA node. This causes ECG changes, which commonly present as retrograde p waves around the QRS complex. [12]

(Reused from Jones, S. A. (2009). ECG Notes: Interpretation and Management Guide. F.A. Davis Company.)

Ventricular arrhythmias are life-threatening conditions that cause sudden cardiac death (SCD); subtypes include monomorphic and polymorphic ventricular tachycardia (VT), Torsades de Pointes (TdP, variant of PVT), ventricular fibrillation (VF). It has been estimated that over 356,000 people suffer from out-of-hospital cardiac arrest in the USA annually, nearly 1000 cases each day [13], and SCD remains the world’s leading cause of death, costing 17 million lives each year [14]. Over the years, VT/VF has decreased incidence; they account for 23% of initial cardiac arrest rhythm, with the most commonly encountered ones being asystole (39%) and PEA (37%). This trend is likely due to the advancement of devices like implantable cardiac defibrillators and improvement in preventative cardiology practice [15]. The most common causes of VT/VF include acute coronary syndrome, cardiomyopathies, congenital channelopathies (BrS, LQTS, CPVT), QT-prolonging drugs (macrolides, TCA), electrolytes imbalance, etc. (Consider 4H 4T causes in cardiac arrest).

(Reused from Jones, S. A. (2009). ECG Notes: Interpretation and Management Guide. F.A. Davis Company.)
(Reused from Jones, S. A. (2009). ECG Notes: Interpretation and Management Guide. F.A. Davis Company.)
(Reused from Jones, S. A. (2009). ECG Notes: Interpretation and Management Guide. F.A. Davis Company.)
(Reused from Jones, S. A. (2009). ECG Notes: Interpretation and Management Guide. F.A. Davis Company.)

The diagram below shows a decision-making algorithm.

(Reused from Srinivasan C, Balaji S. Neonatal supraventricular tachycardia. Indian Pacing Electrophysiol J. 2019;19(6):222-231. DOI:10.1016/j.ipej.2019.09.004) – Open Access (https://www.sciencedirect.com/science/article/pii/S0972629219301159)

Medical History

As tachyarrhythmias present with an extensive list of differential diagnoses, a detailed history taking is essential to direct clinicians to the next-step management. The most common clinical presentations in patients suffering from tachycardias include palpitations (84%), chest pain (47%), dyspnoea (38%), syncope (26%), light-headedness (19%) and sweating (18%) [16]. Symptoms can be explored with a simple mnemonic SOCRATES (site/specify, onset, character/change, rhythm/radiation, associated features, timing, exacerbating and relieving factors, severity). As patients often confuse medical terms with other meanings, it is important to ask and clarify what the term means to them (palpitations vs heart attack). Understanding the onset and progression of symptoms would allow us to determine the acuity and chronicity of the presentation. For timing, we need to ask if the presentation constantly existed since the onset, if it is intermittent, and if it comes on at a particular time of the day. In terms of exacerbating and relieving factors, when it comes to cardiac problems, it is particularly important to ask about the difference between exertion and rest and whether the patient tried anything over the counter. As non-cardiac problems cause tachycardia too, it is necessary to perform a systems review from head to toe to rule out other causes (for example, diarrhea, weight loss, heat intolerance, menstrual disturbance in hyperthyroidism). Past medical and family history should never be missed; these help us to identify risk factors, e.g., hypertension, diabetes, familial hypercholesteremia (predispose to MI), and HOCM (predispose to SCD). In the end, remember to ask for medication history (both prescribed and illicit) and social history (especially smoking and alcohol intake).

If the patient is unconscious, collateral histories from friends and family members are ideal candidates to gain some basic understanding of the patient’s background. It is also worthwhile to communicate with EMTs and paramedics and see if any other valuable information can be obtained.

Adverse features (red flags) for tachyarrhythmias are mainly myocardial infarction, syncope, new-onset heart failure, and deteriorating vital signs, i.e., increased capillary refill time, hypotension (indicative of shock), altered consciousness/reduced GCS.

Physical Examination

If the patient is unconscious or has no palpable pulse, manage the patient with basic life support and advanced life support protocols.

Evaluation of all other patients with the A-E approach is critical as they are still undifferentiated. If the patient is conscious, start inspecting the patient. Key features to observe include cyanosis (poor perfusion peri-arrest), pallor (anemia), dyspnea (heart failure, myocardial infarction/injury), diaphoresis (myocardial infarction/injury), and peripheral edema (heart failure). Start peripherally at hands, observe for clubbing (indicative of infective endocarditis, congenital heart diseases, hyperthyroidism), and assess radial and carotid pulse for its rate, rhythm, and volume. Look for visible jugular venous pulse (elevated – heart failure), presence of corneal arcus (familial hypercholesterolemia) in eyes, and scars on the chest (sternotomy, pacemaker). To assess murmurs, auscultate in all 4 valvular areas (2ndICS left sternal border – pulmonary area, 2nd ICS, right sternal border – aortic area, 4th ICS left sternal border – tricuspid area, 5th ICS mid-clavicular line – mitral area). Be sure to examine other systems, including respiratory, neurological, and ENT.

Alternative Diagnoses

As mentioned above, most tachyarrhythmias are idiopathic or secondary to cardiac and non-cardiac causes. It is extremely important to keep an open mind and an extensive list of differentials so we won’t miss the actual diagnosis. The table below lists differentials for palpitations, the chief complaint of tachyarrhythmias.

Causes of Palpitations

Cardiac Causes

Noncardiac Causes

Atrial fibrillation/flutter

Atrial myxoma

Atrial premature contractions

Atrioventricular reentry

Atrioventricular tachycardia

Autonomic dysfunction

Cardiomyopathy

Long QT syndrome

Multifocal atrial tachycardia

Sick sinus syndrome

Supraventricular tachycardia

Valvular heart disease

Ventricular premature contractions

Ventricular tachycardia

Alcohol

Anemia

Anxiety/stress

Beta-blocker withdrawal

Caffeine

Cocaine

Exercise

Fever

Medications

Nicotine

Paget disease of bone

Pheochromocytoma

Pregnancy

Thyroid dysfunction

(Reuse from Wexler RK, Pleister A, Raman SV. Palpitations: Evaluation in the Primary Care Setting. Am Fam Physician. 2017;96(12):784-789.) – Open Access (https://www.aafp.org/pubs/afp/issues/2017/1215/p784.html)

Acing Diagnostic Testing

Any patients with adverse features and life-threatening presentations should be placed in a resuscitation bay with a multi-parameter vitals monitor/defibrillator connected and a point-of-care portable ultrasound ready. For stable patients, stepwise management should be initiated. Proceed with bedside tests: perform a 12-lead ECG, measure heart rate, assess SpO2 with an oximeter, and record blood pressure. Collect blood samples, including a Full Blood Count, Urea and Electrolytes, serum Magnesium, Calcium, Thyroid Function Tests, Liver Function Tests, and a coagulation panel. Additional tests can be considered based on the clinician’s clinical decision and the patient’s presentation, for example, Troponin for suspected MI, D-dimer for suspected PE, etc. Chest X-rays should be performed in any patients presenting with chest pain. Advanced imaging again depends on clinical presentation, coronary angiogram for Myocardial Infarction, Computed Tomography Pulmonary Angiography for Pulmonary Embolism, etc. The risk stratification tool (more details in the section below) can be used to facilitate decisions for advanced interventions involving intensive care input. Cardiology input will be required for further investigations involving Holter monitoring, implantable loop recorder, electrophysiological study, echocardiogram, cardiac Magnetic Resonance Imaging, etc.

Management

Sinus Tachycardia

Sinus tachycardia is often a physiological response to an underlying cause such as sepsis, hypovolemia, or anemia. Management should focus on identifying and addressing these causes rather than targeting the heart rate itself. For example, in a septic patient, early fluid resuscitation and antibiotics are critical, while in a patient with anemia, blood transfusion or treatment of iron deficiency may resolve the tachycardia. Clinicians should avoid unnecessary use of beta-blockers or calcium channel blockers unless sinus tachycardia persists after the underlying cause has been addressed.

Atrial Fibrillation

Management of atrial fibrillation requires a careful evaluation of the patient’s hemodynamic stability, symptom duration, and underlying comorbidities.

  1. Hemodynamically Stable Patients with Symptoms >48 Hours or Uncertain Timeline:

    • Rate control is the priority to prevent further decompensation. Start with beta-blockers (e.g., bisoprolol) or calcium channel blockers (e.g., diltiazem).
    • Consider digoxin for patients with congestive heart failure who may not tolerate beta-blockers.
    • Avoid cardioversion without anticoagulation if the symptom duration is >48 hours or unclear, as this increases the risk of thromboembolic events.

  2. Hemodynamically Stable Patients with Symptoms <48 Hours or a Reversible Cause:

    • Focus on rhythm control with cardioversion, which can be electrical or pharmacological (e.g., flecainide or amiodarone).
    • Ensure anticoagulation with heparin before cardioversion unless contraindicated.
    • Use an echocardiogram to rule out structural abnormalities, as this guides drug selection (e.g., flecainide for structurally normal hearts; amiodarone for structural heart disease).

  3. Patients with Adverse Features (Shock, Syncope, Acute Heart Failure, or Myocardial Ischemia):

    • Immediate electrical cardioversion is required, typically using synchronized shocks. Time is critical—any delay could worsen outcomes.

  4. Paroxysmal AF:

    • Counsel patients on the use of “pill-in-the-pocket” therapies such as flecainide or sotalol for intermittent symptoms. Ensure they understand the signs of structural heart disease, which would contraindicate these medications.

Always consider underlying conditions such as hyperthyroidism, electrolyte disturbances, or alcohol-related atrial fibrillation (Holiday Heart Syndrome). Addressing these causes can prevent recurrence. In elderly patients or those with heart failure, weigh the benefits of rhythm versus rate control.

Atrial Flutter

Management of atrial flutter parallels that of atrial fibrillation. Rate control is often sufficient in stable patients, but rhythm control may be prioritized for symptomatic relief. In acute settings, electrical cardioversion may be more effective than pharmacological approaches.

Atrial flutter is frequently associated with underlying structural heart disease or atrial enlargement. Evaluate for these conditions with echocardiography and address them to improve long-term outcomes.

AVNRT (Atrioventricular Nodal Reentrant Tachycardia)

AVNRT is often well-managed with non-pharmacological measures in stable patients.

Conservative Management:

  • Initiate vagal maneuvers (e.g., Valsalva maneuver or carotid massage). These can terminate the tachycardia in many cases. Ensure the patient is monitored for safety, especially in older adults where carotid massage could induce complications.

Pharmacological Management:

  • Administer IV adenosine, starting at 6 mg and escalating to 12 mg or 18 mg if needed. Warn the patient about the transient sensation of chest discomfort or flushing.
  • If adenosine is contraindicated (e.g., in asthmatic patients), use a calcium channel blocker such as verapamil.

Persistent Cases:

  • Consider beta-blockers, digoxin, or amiodarone if initial treatments fail.

Hemodynamically Unstable Patients:

  • Proceed with immediate cardioversion to stabilize the patient.

In recurrent AVNRT, evaluate for underlying triggers such as excessive caffeine or stimulant use. Discuss long-term options such as catheter ablation for definitive treatment.

AVRT/WPW (Atrioventricular Reentrant Tachycardia/Wolff-Parkinson-White Syndrome)

In patients with WPW, rapid and accurate diagnosis is critical to avoid inappropriate treatment.

Stable Patients:

  • Treat with amiodarone, flecainide, or procainamide. Avoid digoxin and calcium channel blockers, as these can worsen pre-excitation and lead to ventricular fibrillation.

Unstable Patients:

  • Immediate cardioversion is indicated.

In young patients presenting with sudden palpitations and syncope, always consider WPW and obtain a 12-lead ECG for diagnosis. Educate patients on avoiding stimulants that may precipitate episodes.

Atrial Tachycardia

For atrial tachycardia, management depends on the patient’s stability. Rate control is often effective for stable patients, while cardioversion may be required in unstable cases.

Investigate underlying causes such as digoxin toxicity or structural heart disease, as addressing these may resolve the tachycardia.

Ventricular Tachycardia (VT)

Management of VT hinges on the patient’s hemodynamic stability.

Stable VT:

    • Administer amiodarone (300 mg IV STAT followed by a 900 mg infusion over 24 hours). Monitor for potential side effects such as hypotension or bradycardia.

Unstable VT, pulse positive:

    • Follow the ALS (Advanced Life Support) algorithm, prioritizing cardioversion.

VT, no pulse:

  • Follow the ALS (Advanced Life Support) algorithm, prioritizing defibrillation and CPR.

In patients with recurrent VT, assess for underlying ischemic heart disease or electrolyte abnormalities. Long-term management may require ICD placement or catheter ablation.

Ventricular Fibrillation (VF)

VF is a life-threatening emergency requiring immediate intervention. Follow the ALS algorithm, which includes high-quality CPR and defibrillation.

Always assess for reversible causes of VF, such as acute myocardial infarction or electrolyte imbalances (e.g., hypokalemia or hypomagnesemia), and treat these aggressively to prevent recurrence.

Tachycardia and advanced life support algorithms are provided below.

(Reuse from Soar J, Böttiger BW, Carli P, et al. European Resuscitation Council Guidelines 2021: Adult advanced life support [published correction appears in Resuscitation. 2021 Oct;167:105-106]. Resuscitation. 2021;161:115-151. DOI:10.1016/j.resuscitation.2021.02.010) – Open Access (https://www.cprguidelines.eu/)
(Reuse from Soar J, Böttiger BW, Carli P, et al. European Resuscitation Council Guidelines 2021: Adult advanced life support [published correction appears in Resuscitation. 2021 Oct;167:105-106]. Resuscitation. 2021;161:115-151. DOI:10.1016/j.resuscitation.2021.02.010) – Open Access (https://www.cprguidelines.eu/)

Special Patient Groups

The management of most tachyarrhythmias is similar among pregnant women and pediatric populations, with the exception of ventricular cardiac arrest rhythms.

Pregnant Patients (Obstetric Cardiac Arrest ) [17]

  • A normal supine position will result in aortocaval compression from the gravid uterus; this reduces cardiac output. Hence, placing the patient in a left lateral position is crucial, especially at> 20 weeks gestation.
  • The position of the rescuer’s hands for chest compression ideally should be slightly higher than usual, taking the elevation of the diaphragm and abdominal contents caused by the gravid uterus into account.
  • The defibrillator pad position should be adjusted to maintain the left lateral position.
  • Magnesium sulfate (4 g IV) should be given in patients with eclampsia.
  • Patients should be intubated early due to the higher risk of pulmonary aspiration and Mendelson syndrome from gastric contents.
  • Emergency delivery of the fetus (>20 weeks) with resuscitative hysterotomy should happen within 5 minutes in the event of cardiac arrest, given that the initial resuscitation attempt has failed. This is a definitive procedure to decompress IVC to facilitate venous return and increase cardiac output.
  • As this is an obstetric emergency, get help from the OB/GYN and neonatal team early; resuscitative hysterotomy should not wait even if not all surgical equipment is immediately available; one scalpel is enough to start the procedure.

Pediatrics (Cardiac Arrest) [17]

  • Most pediatric cardiac arrests are secondary to respiratory failure; hence, giving 5 rescue breaths is essential prior to chest compressions.
  • Pulse checks use brachial or femoral pulses as opposed to carotid pulses in adults.
  • It is a similar compression site but with a compression: breath ratio of 15:2, as opposed to 30:2 in adults.
  • In infants, compress the chest using two fingers or an encircling technique (two thumbs). For children over one year old, use one or two hands.
  • Intraosseous (IO) access is preferred for circulation access, as obtaining venous access can be difficult in children.
  • Adrenaline is given in 10 mcg/kg, and Amiodarone is given in 5 mg/kg.
  • Note that PALS is different from newborn life support (NLS), which is not mentioned here.

* Please refer to European Resuscitation Council (ERC) Paediatric Life Support and Special Circumstances Guidelines (https://www.cprguidelines.eu/)

Risk Stratification

There is no single risk stratification tool for tachyarrhythmias, developed scoring systems are usually condition-specific or presentation-specific. We listed some of the important ones related to tachyarrhythmias below:

  • Cardiac Arrest Hospital Prognosis (CAHP) score – predicts prognosis in patients suffering from out-of-hospital cardiac arrest. [18]
  • Cardiac Arrest Risk Triage (CART) Score – predicts the risk of in-hospital cardiac arrest in hospitalized patients. [19]
  • CHA₂DS₂-VASc Score – calculate stroke risk in patients with atrial fibrillation and guide initiation of anticoagulation therapy. [20]
  • HEART score – predicts patients presenting with chest pain for a 6-week risk of major adverse cardiac events (MACE). It can also classify patients into low, moderate, and high-risk groups to facilitate decisions for discharge from ED, admission for observation, or urgent intervention required. [21]
  • Thrombolysis In Myocardial Infarction (TIMI) score and Global Registry of Acute Coronary Events (GRACE) score – estimate mortality for patients with acute coronary syndrome, guide decision for coronary revascularisation needs. [22]
  • Well’s Score – calculate the clinical probability of DVT/PE and guide the decision to consider alternative diagnosis or perform immediate CTPA/anticoagulation. [23]
  • Pulmonary Embolism Rule Out Criteria (PERC) – effectively rules out PE if scored 0. [24]
  • Pulmonary Embolism Severity Index (PESI) – predicts 30-day mortality in patients with PE. [25]
  • Emergency Heart Failure Mortality Risk Grade (EHMRG) estimates 7-day mortality in patients with congestive heart failure and guides the decision to admit them [26].
  • San Francisco syncope rule (SFSR), Canadian syncope risk score (CSRS), and Evaluation of Guidelines in SYncope Study (EGSYS) Score – both SFSR and CSRS predict adverse outcomes in patients presenting with syncope (7-day and 30-day, respectively), EGSYS helps determine whether syncope is cardiac or non-cardiac cause (these includes vasovagal, situational, postural hypotension). [27-29]
  • Multi-parametric models – predict the prognosis of patients with Brugada syndrome for future major arrhythmic events (VT/VF) and guide decisions for implantable cardioverter defibrillator placement. [30]

* Please browse these calculators on MDCalc website (https://www.mdcalc.com/)

When To Admit This Patient

Patients with adverse features and hemodynamic instability require immediate intervention and admission. The aforementioned risk stratification tools can be used based on clinical signs and symptoms. If initial investigations yielded no clinical significance, patients could be discharged with education, reassurance, and safety netting advice. Explain that palpitations are usually transient and harmless; if they are recurring, ask patients to note down the onset, timing, and duration and measure BP and HR if monitoring is available at home. Advise them to reattend ED if symptoms persist or worsen or new-onset red flag symptoms emerge; lifestyle advice, for example, avoid certain known stimulants like caffeine, alcohol, and nicotine. If the patient is known to have SVT, educate about self-performing Valsalva maneuver to try terminating it before medical assistance arrives. Arrange follow-up with a family physician and review the need for further investigations and specialist input. Patients should be referred urgently for detailed investigations, including Holter monitoring if non-specific new clinical findings are yielded. Other options may be explored, such as an echocardiogram, implantable loop recorder, and electrophysiology study. [31, 32]

Revisiting Your Patient

The case reminds us that tachyarrhythmias can be secondary to non-cardiac causes. This is a classical presentation of hyperthyroidism, with ECG showing fast-rate atrial fibrillation. Atrial fibrillation occurs in 15% of patients with hyperthyroidism. A detailed history taking with appropriate systems review (as symptoms suggest) would point us towards hyperthyroidism. Clinical examination may reveal clubbing (thyroid acropachy), exomphalos (thyroid eye disease), pretibial myxoedema, goiter, and an irregular heartbeat with mid-systolic scratchy murmur (Means–Lerman scratch) might be heard on auscultation. The investigation here, starting from bedside, would be to obtain a complete set of vital signs (blood pressure, heart rate, respiratory rate, temperature, SpO2), 3-lead continuous monitoring, and 12-lead ECG; blood including complete blood count, urea and electrolytes, thyroid function tests, troponin (serial), venous blood gas, other electrolytes (Ca2+). The management approach of this patient is to treat the underlying hyperthyroidism primarily. Hence, endocrinologist referral will be required, with cardiologists’ input on managing the fast Atrial Fibrillation. Propranolol (reduces peripheral conversion of T4 to T3) and anti-thyroid drugs like carbimazole (inhibits thyroid peroxidase action) are the mainstay management (details see thyroid disorder chapter). However, as the patient also complains of anginal pain, rate control with cardio-selective beta-blockers should be initiated as well. It also helps with alleviating symptoms of hyperthyroidism, including palpitations, tremors, anxiety, heat intolerance, etc., due to the increased sympathetic tone caused by excess thyroid hormone production. The need for anticoagulation is assessed on an individual basis. In most cases, Atrial Fibrillation reverses to sinus rhythm spontaneously after the euthyroid state has been achieved. However, if Atrial Fibrillation persists, cardioversion may be considered. This, nevertheless, would be a cardiologist’s decision. [33]

Authors

Picture of Keith Sai Kit Leung

Keith Sai Kit Leung

Keith is an academic foundation doctor (emergency medicine themed) in the UK. He graduated both BSc and MBChB with distinction, and has published over 30 peer-reviewed articles till date. He is interested in Pre-Hospital Emergency & Retrieval Medicine, Intensive Care, Cardiology and Medical Education. He main research interests are arrhythmias and cardiac electrophysiology, cardiac arrest and resuscitation, ACS, POCUS, ECMO, airway and trauma management. He aims to work as an academic PHEM/HEMS physician and pursue a MD (Res)/PhD in the near future.

Picture of Rafaqat Hussain

Rafaqat Hussain

Dr Rafaqat Hussain is working as Specialty Doctor in Emergency Department at SWBH NHS trust. He had done MBBS.MRCEM. FRCEM.EBCEM. He has involved in training and teaching for junior doctors and medical students at University of Birmingham. He is enthusiastic in pursuing his career in being an Emergency Medicine Consultant.

Picture of Abraham Ka Cheung Wai

Abraham Ka Cheung Wai

Dr Abraham Wai, Clinical Associate Professor at the University of Hong Kong (HKU), is a dynamic force in the field of emergency medicine. His journey from specialist training to impactful research and innovative teaching has left an indelible mark on the healthcare landscape.

Listen to the chapter

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Reviewed and Edited By

Picture of Arif Alper Cevik, MD, FEMAT, FIFEM

Arif Alper Cevik, MD, FEMAT, FIFEM

Prof Cevik is an Emergency Medicine academician at United Arab Emirates University, interested in international emergency medicine, emergency medicine education, medical education, point of care ultrasound and trauma. He is the founder and director of the International Emergency Medicine Education Project – iem-student.org, chair of the International Federation for Emergency Medicine (IFEM) core curriculum and education committee and board member of the Asian Society for Emergency Medicine and Emirati Board of Emergency Medicine.